start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=12 article-no= start-page=002177 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20251217 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Thorough characterization of a new curvulavirid from a Japanese strain of Cryphonectria nitschkei en-subtitle= kn-subtitle= en-abstract= kn-abstract=A new curvulavirid was isolated from a Japanese strain of the filamentous ascomycete Cryphonectria nitschkei and thoroughly characterized. The virus termed Cryphonectria nitschkei curvulavirus 1 (CnCvV1) has a bi-segmented dsRNA genome. CnCvV1 dsRNA1 encodes an RNA-dependent RNA polymerase (592 amino acids), while dsRNA2 possesses two ORFs, one that encodes a protein associated with the genomic dsRNA and the other that encodes a hypothetical protein of unknown function. CnCvV1 could be experimentally introduced into another virus-free strain of C. nitschkei and two strains of different fungal species within the genus Cryphonectria (Cryphonectria parasitica and Cryphonectria carpinicola). Based on phenotypic comparison, the virus caused asymptomatic infection in the three newly established fungal strains. However, there was a reduced colony growth rate and increased CnCvV1 accumulation in an RNA silencing-deficient mutant (Δdcl2), relative to the wt strain EP155 of a model virus host fungus (C. parasitica). These findings suggest that CnCvV1 is targeted by RNA silencing in C. parasitica. This study provides a foundation for further exploration of curvulavirids that have been biologically understudied. en-copyright= kn-copyright= en-aut-name=ShahiSabitree en-aut-sei=Shahi en-aut-mei=Sabitree kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HisanoSakae en-aut-sei=Hisano en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Sa'diyahWasiatus en-aut-sei=Sa'diyah en-aut-mei=Wasiatus kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakakiYoshihiro en-aut-sei=Takaki en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=?Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=?Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=?Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=?Institute for Extra-cutting-edge Science and Technology Avant-garde Research (X-star), Japan Agency for Marine-Earth Science and Technology (JAMSTEC) kn-affil= affil-num=5 en-affil=?Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=6 en-affil=?Institute of Plant Science and Resources, Okayama University kn-affil= en-keyword=curvulavirus kn-keyword=curvulavirus en-keyword=Cryphonectria carpinicola kn-keyword=Cryphonectria carpinicola en-keyword=Cryphonectria nitschkei kn-keyword=Cryphonectria nitschkei en-keyword=Cryphonectria parasitica kn-keyword=Cryphonectria parasitica en-keyword=fungal dsRNA virus kn-keyword=fungal dsRNA virus en-keyword=host range kn-keyword=host range en-keyword=RNA silencing kn-keyword=RNA silencing END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7 article-no= start-page=002115 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250725 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses (ICTV) from the Fungal and Protist Viruses Subcommittee, 2025 en-subtitle= kn-subtitle= en-abstract= kn-abstract=The Fungal and Protist Viruses Subcommittee (SC) of the International Committee on Taxonomy of Viruses (ICTV) has received a total of eight taxonomic proposals for the 2024 annual cycle. The extent of proposed changes varied, including nomenclatural updates, creation of new taxa and reorganization of established taxa. Following the ICTV procedures, all proposals were reviewed and voted upon by the members of the Executive Committee with ratification in March 2025. As a result, a total of 52 species in the families Botourmiaviridae and Marnaviridae were renamed to comply with the mandated binomial format. A new genus has been added to the dsRNA virus family Amalgaviridae, while two new families, Splipalmiviridae (Wolframvirales) and Mycoalphaviridae (Hepelivirales), were created to classify new groups of positive-sense (+) RNA mycoviruses. The class Arfiviricetes (Cressdnaviricota) was expanded by a new order Lineavirales and a new family Oomyviridae of ssDNA viruses. Additionally, a new class Orpoviricetes was created in the kingdom Orthornavirae to classify a group of bisegmented (+)RNA viruses reported from fungi and oomycetes. Finally, the order Pimascovirales was reorganized to better depict evolutionary relationships of pithoviruses and related viruses with large dsDNA genomes. The summary of updates in the taxonomy of fungal and protist viruses presented here is limited to taxa within the remit of this Subcommittee. For information on taxonomy changes on other fungal viruses closely related to animal and/or plant viruses, please see reports from sister ICTV Subcommittees (i.e. Plant Virus SC and Animal dsRNA and ssRNA(?) Viruses SC). en-copyright= kn-copyright= en-aut-name=SabanadzovicSead en-aut-sei=Sabanadzovic en-aut-mei=Sead kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AbergelChantal en-aut-sei=Abergel en-aut-mei=Chantal kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Ayll?nMar??a A. en-aut-sei=Ayll?n en-aut-mei=Mar??a A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=BotellaLeticia en-aut-sei=Botella en-aut-mei=Leticia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=CanutiMarta en-aut-sei=Canuti en-aut-mei=Marta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChibaYuto en-aut-sei=Chiba en-aut-mei=Yuto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ClaverieJean-Michel en-aut-sei=Claverie en-aut-mei=Jean-Michel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=CouttsRobert H.A. en-aut-sei=Coutts en-aut-mei=Robert H.A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=DaghinoStefania en-aut-sei=Daghino en-aut-mei=Stefania kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=DonaireLivia en-aut-sei=Donaire en-aut-mei=Livia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=ForgiaMarco en-aut-sei=Forgia en-aut-mei=Marco kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=HejnaOnd?ej en-aut-sei=Hejna en-aut-mei=Ond?ej kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=JiaJichun en-aut-sei=Jia en-aut-mei=Jichun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=JiangDaohong en-aut-sei=Jiang en-aut-mei=Daohong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=Kotta-LoizouIoly en-aut-sei=Kotta-Loizou en-aut-mei=Ioly kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=KrupovicMart en-aut-sei=Krupovic en-aut-mei=Mart kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=LangAndrew S. en-aut-sei=Lang en-aut-mei=Andrew S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=LegendreMatthieu en-aut-sei=Legendre en-aut-mei=Matthieu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=Lee MarzanoShin-Yi en-aut-sei=Lee Marzano en-aut-mei=Shin-Yi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=NervaLuca en-aut-sei=Nerva en-aut-mei=Luca kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=P?nzesJudit en-aut-sei=P?nzes en-aut-mei=Judit kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=PoimalaAnna en-aut-sei=Poimala en-aut-mei=Anna kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=RigouSofia en-aut-sei=Rigou en-aut-mei=Sofia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=SatoYukiyo en-aut-sei=Sato en-aut-mei=Yukiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=ShamsiWajeeha en-aut-sei=Shamsi en-aut-mei=Wajeeha kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=26 ORCID= en-aut-name=TurinaMassimo en-aut-sei=Turina en-aut-mei=Massimo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=27 ORCID= en-aut-name=UrayamaSyun-ichi en-aut-sei=Urayama en-aut-mei=Syun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=28 ORCID= en-aut-name=VainioEeva J. en-aut-sei=Vainio en-aut-mei=Eeva J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=29 ORCID= en-aut-name=XieJiatao en-aut-sei=Xie en-aut-mei=Jiatao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=30 ORCID= affil-num=1 en-affil=Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University kn-affil= affil-num=2 en-affil=Information G?nomique & Structurale, UMR7256, CNRS & Aix-Marseille Universit?, Marseille, IMM, IM2B, IOM kn-affil= affil-num=3 en-affil=Departamento de Biotecnolog?a-Biolog?a Vegetal, Escuela T?cnica Superior de Ingenier?a Agron?mica, Alimentaria y de Biosistemas, Universidad Polit?cnica de Madrid (UPM) kn-affil= affil-num=4 en-affil=Forest Protection and Wildlife Management Mendel University in Brno kn-affil= affil-num=5 en-affil=Department of Veterinary and Animal Sciences, University of Copenhagen kn-affil= affil-num=6 en-affil=School of Agriculture, Meiji University kn-affil= affil-num=7 en-affil=Information G?nomique & Structurale, UMR7256, CNRS & Aix-Marseille Universit?, Marseille, IMM, IM2B, IOM kn-affil= affil-num=8 en-affil=School of Health, Medicine and Life Sciences, University of Hertfordshire kn-affil= affil-num=9 en-affil=Institute for Sustainable Plant Protection, National Research Council of Italy kn-affil= affil-num=10 en-affil=Centro de Edafolog?a y Biolog?a Aplicada del Segura-CSIC kn-affil= affil-num=11 en-affil=Institute for Sustainable Plant Protection, CNR kn-affil= affil-num=12 en-affil=Department of Genetics and Biotechnologies, University of South Bohemia kn-affil= affil-num=13 en-affil=College of Plant Protection, Shanxi Agricultural University kn-affil= affil-num=14 en-affil=College of Plant Science and Technology, Huazhong Agricultural University kn-affil= affil-num=15 en-affil=School of Health, Medicine and Life Sciences, University of Hertfordshire kn-affil= affil-num=16 en-affil=Institut Pasteur, Universit? Paris Cit?, CNRS UMR6047, Archaeal Virology Unit kn-affil= affil-num=17 en-affil=Department of Biology, Memorial University of Newfoundland kn-affil= affil-num=18 en-affil=Information G?nomique & Structurale, UMR7256, CNRS & Aix-Marseille Universit?, Marseille, IMM, IM2B, IOM kn-affil= affil-num=19 en-affil=United States Department of Agriculture, Agricultural Research Service, Application Technology Research Unit kn-affil= affil-num=20 en-affil=Council for Agricultural Research and Economics - Research Centre for Viticulture and Enology kn-affil= affil-num=21 en-affil=Department of Entomology, Texas A&M University kn-affil= affil-num=22 en-affil=Natural Resources Institute Finland (Luke) kn-affil= affil-num=23 en-affil=Information G?nomique & Structurale, UMR7256, CNRS & Aix-Marseille Universit?, Marseille, IMM, IM2B, IOM kn-affil= affil-num=24 en-affil=Department of Biology, Institute for Plant Sciences, University of Cologne kn-affil= affil-num=25 en-affil=Department of Molecular Biology and Genetics, Aarhus University kn-affil= affil-num=26 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=27 en-affil=Department of Plant Protection, School of Agriculture, The University of Jordan kn-affil= affil-num=28 en-affil=Department of Life and Environmental Sciences, University of Tsukuba kn-affil= affil-num=29 en-affil=Natural Resources Institute Finland (Luke) kn-affil= affil-num=30 en-affil=College of Plant Science and Technology, Huazhong Agricultural University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7 article-no= start-page=002079 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250725 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Virus taxonomy proposal summaries: a searchable and citable resource to disseminate virus taxonomy advances en-subtitle= kn-subtitle= en-abstract= kn-abstract=Taxonomic classification of cellular organisms requires the publication of descriptions and proposed names of species and the deposition of specimens. Virus taxonomy is developed through a different system of annual submission of formal taxonomy proposals (TPs) that can be submitted by anyone but are typically prepared by a study group appointed by the International Committee on Taxonomy of Viruses (ICTV) and consisting of experts on a particular group of viruses. These are initially evaluated by an expert subcommittee and by the executive committee (EC) of the ICTV. EC-approved TPs are then submitted for evaluation and a ratification vote by the wider ICTV membership. Following ratification, the new taxonomy is annually updated in the Master Species List, associated databases and bioinformatic resources. The process is consistent, creates traceability in assignments and supports a fully evaluated, hierarchical classification and nomenclature of all taxonomic ranks from species to realms. The structure also facilitates large-scale and coordinated changes to virus taxonomy, such as the recent introduction of a binomial species nomenclature.
TPs are available on the ICTV website after ratification, but they are not indexed in bibliographic databases and are not easily cited. Authors of TPs do not receive citation credit for adopted proposals, and their voluntary contributions are largely invisible in the published literature. For greater visibility of TPs and their authors, the ICTV will commence the annual publication of summaries of all TPs from each ICTV subcommittee. These summaries will provide a searchable compendium of all annual taxonomy changes and additions as well as direct links to the Master Species List and other ICTV bioinformatic resources. Their publication will provide due credit and citations for their authors, form the basis for disseminating taxonomy decisions and promote greater visibility and accessibility to taxonomy changes for the virology community. en-copyright= kn-copyright= en-aut-name=MayneRichard en-aut-sei=Mayne en-aut-mei=Richard kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SimmondsPeter en-aut-sei=Simmonds en-aut-mei=Peter kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SmithDonald B. en-aut-sei=Smith en-aut-mei=Donald B. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=AdriaenssensEvelien M. en-aut-sei=Adriaenssens en-aut-mei=Evelien M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=LefkowitzElliot J. en-aut-sei=Lefkowitz en-aut-mei=Elliot J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OksanenHanna M. en-aut-sei=Oksanen en-aut-mei=Hanna M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ZerbiniFrancisco Murilo en-aut-sei=Zerbini en-aut-mei=Francisco Murilo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=Alfenas-ZerbiniPoliane en-aut-sei=Alfenas-Zerbini en-aut-mei=Poliane kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=AylwardFrank O en-aut-sei=Aylward en-aut-mei=Frank O kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=Freitas-Ast?aJuliana en-aut-sei=Freitas-Ast?a en-aut-mei=Juliana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=HendricksonR. Curtis en-aut-sei=Hendrickson en-aut-mei=R. Curtis kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=HughesHolly R. en-aut-sei=Hughes en-aut-mei=Holly R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KrupovicMart en-aut-sei=Krupovic en-aut-mei=Mart kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=KuhnJens H. en-aut-sei=Kuhn en-aut-mei=Jens H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=?obockaMa?gorzata en-aut-sei=?obocka en-aut-mei=Ma?gorzata kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=MushegianArcady R. en-aut-sei=Mushegian en-aut-mei=Arcady R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=PenzesJudit en-aut-sei=Penzes en-aut-mei=Judit kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=Mu?ozAlejandro Reyes en-aut-sei=Mu?oz en-aut-mei=Alejandro Reyes kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=RobertsonDavid L. en-aut-sei=Robertson en-aut-mei=David L. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=RouxSimon en-aut-sei=Roux en-aut-mei=Simon kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=RubinoLuisa en-aut-sei=Rubino en-aut-mei=Luisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=SabanadzovicSead en-aut-sei=Sabanadzovic en-aut-mei=Sead kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=TurnerDann en-aut-sei=Turner en-aut-mei=Dann kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=Van DoorslaerKoenraad en-aut-sei=Van Doorslaer en-aut-mei=Koenraad kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= en-aut-name=VarsaniArvind en-aut-sei=Varsani en-aut-mei=Arvind kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=26 ORCID= affil-num=1 en-affil=Nuffield Department of Medicine, University of Oxford kn-affil= affil-num=2 en-affil=Nuffield Department of Medicine, University of Oxford kn-affil= affil-num=3 en-affil=Nuffield Department of Medicine, University of Oxford kn-affil= affil-num=4 en-affil=Quadram Institute Bioscience kn-affil= affil-num=5 en-affil=Department of Microbiology, University of Alabama at Birmingham kn-affil= affil-num=6 en-affil=Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki kn-affil= affil-num=7 en-affil=Departamento de Fitopatologia/BIOAGRO, Universidade Federal de Vi?osa kn-affil= affil-num=8 en-affil=Departamento de Microbiologia, Universidade Federal de Vi?osa kn-affil= affil-num=9 en-affil=Department of Biological Sciences, Virginia Tech kn-affil= affil-num=10 en-affil=Embrapa Cassava and Fruits, Cruz das Almas kn-affil= affil-num=11 en-affil=Department of Microbiology, University of Alabama at Birmingham kn-affil= affil-num=12 en-affil=Centers for Disease Control and Prevention kn-affil= affil-num=13 en-affil=Institut Pasteur, Universit? Paris Cit?, CNRS UMR6047, Archaeal Virology Unit kn-affil= affil-num=14 en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health kn-affil= affil-num=15 en-affil=Institute of Biochemistry and Biophysics of the Polish Academy of Sciences kn-affil= affil-num=16 en-affil=Division of Molecular and Cellular Biosciences, National Science Foundation kn-affil= affil-num=17 en-affil=Institute for Quantitative Biomedicine, Rutgers University kn-affil= affil-num=18 en-affil=Departamento de Ciencias Biol?gicas, Universidad de los Andes kn-affil= affil-num=19 en-affil=MRC-University of Glasgow Centre for Virus Research kn-affil= affil-num=20 en-affil=Department of Energy, Joint Genome Institute, Lawrence Berkeley National Laboratory kn-affil= affil-num=21 en-affil=Consiglio Nazionale delle Ricerche, Istituto per la Protezione Sostenibile delle Piante, Sede Secondaria di Bari kn-affil= affil-num=22 en-affil=Department of Agricultural Science and Plant Protection, Mississippi State University kn-affil= affil-num=23 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=24 en-affil=Molecular Biology, University of the West of England kn-affil= affil-num=25 en-affil=Department of Immunobiology, School of Animal and Comparative Biomedical Sciences, BIO5 Institute, University of Arizona Cancer Center kn-affil= affil-num=26 en-affil=The Biodesign Center for Fundamental and Applied Microbiomics, School of Life Sciences, Center for Evolution and Medicine, Arizona State University kn-affil= en-keyword=ICTV kn-keyword=ICTV en-keyword=master species list kn-keyword=master species list en-keyword=taxonomy proposal kn-keyword=taxonomy proposal en-keyword=virus taxonomy kn-keyword=virus taxonomy END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page=e06572 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250908 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A Viral RNA Silencing Suppressor Modulates Reactive Oxygen Species Levels to Induce the Autophagic Degradation of Dicer‐Like and Argonaute‐Like Proteins en-subtitle= kn-subtitle= en-abstract= kn-abstract=Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated. Strikingly, this ROS-induced autophagy selectively targets for degradation two core antiviral RNA silencing components against CHV1 in F. graminearum, Dicer-like 2 (DCL2) and Argonaute-like 1 (AGL1), thereby compromising the host's primary antiviral defense system. Genetic analysis confirms this coordinated hijacking of host machineries, as CHV1 shows enhanced accumulation in the FMR1 knockout and reduced accumulation in autophagy-deficient fungal strains. This work reveals a tripartite interplay among oxidative stress, autophagy, and RNA silencing that CHV1 manipulates through p29 multifunctional activity. These findings provide a model for how viruses coordinately regulate distinct host defense systems to optimize infection. en-copyright= kn-copyright= en-aut-name=ZhaiShiyu en-aut-sei=Zhai en-aut-mei=Shiyu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=PangTianxing en-aut-sei=Pang en-aut-mei=Tianxing kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=PengShiyu en-aut-sei=Peng en-aut-mei=Shiyu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ZouShenshen en-aut-sei=Zou en-aut-mei=Shenshen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=DengZhiping en-aut-sei=Deng en-aut-mei=Zhiping kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KangZhensheng en-aut-sei=Kang en-aut-mei=Zhensheng kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=AndikaIda Bagus en-aut-sei=Andika en-aut-mei=Ida Bagus kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SunLiying en-aut-sei=Sun en-aut-mei=Liying kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= affil-num=2 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= affil-num=3 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= affil-num=4 en-affil=Department of Plant Pathology, College of Plant Protection, Shandong Agricultural University kn-affil= affil-num=5 en-affil=Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=7 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= affil-num=8 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= affil-num=9 en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University kn-affil= en-keyword=argonaute kn-keyword=argonaute en-keyword=autophagic degradation kn-keyword=autophagic degradation en-keyword=cryphonectria hypovirus 1 kn-keyword=cryphonectria hypovirus 1 en-keyword=dicer kn-keyword=dicer en-keyword=reactive oxygen species kn-keyword=reactive oxygen species en-keyword=RNA silencing suppressor kn-keyword=RNA silencing suppressor END start-ver=1.4 cd-journal=joma no-vol=99 cd-vols= no-issue=10 article-no= start-page=e00984-25 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20251023 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Human herpesvirus 6B U65 binds to histone proteins and suppresses interferon production en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human herpesvirus 6B (HHV-6B), a member of the Betaherpesvirinae subfamily, is a T-lymphotropic virus that causes exanthem subitum and has been implicated in neuroinflammatory conditions such as multiple sclerosis. The tegument proteins, which are characteristic of herpesviruses, play a crucial role in the envelopment of virions and evasion of host immune defenses, such as the interferon β (IFNβ) signaling pathway. However, the precise mechanisms through which the HHV-6B tegument proteins modulate the IFNβ pathway are not yet fully understood. In this study, we identified a novel function of the HHV-6B tegument protein U65 as an inhibitor of IFNβ production. Additionally, two host histone proteins, hCG_2039566 (H2ACG) and H2AC7, were identified as positive regulators of innate immune pathways. U65 interacts with H2ACG and H2AC7, impairing their ability to promote the IFNβ pathway. Furthermore, we demonstrated that U65 plays critical roles during HHV-6B infection. This study highlights a critical strategy employed by HHV-6B to evade immune defenses, shedding light on its mechanisms for counteracting host responses. en-copyright= kn-copyright= en-aut-name=LiHaokun en-aut-sei=Li en-aut-mei=Haokun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TengDa en-aut-sei=Teng en-aut-mei=Da kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OkameYuki en-aut-sei=Okame en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NambaHikaru en-aut-sei=Namba en-aut-mei=Hikaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=HHV-6B kn-keyword=HHV-6B en-keyword=interferons kn-keyword=interferons en-keyword=histone kn-keyword=histone en-keyword=tegument kn-keyword=tegument en-keyword=U65 kn-keyword=U65 END start-ver=1.4 cd-journal=joma no-vol=15 cd-vols= no-issue=1 article-no= start-page=7661 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2024 dt-pub=20240916 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Neurotransmitter recognition by human vesicular monoamine transporter 2 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human vesicular monoamine transporter 2 (VMAT2), a member of the SLC18 family, plays a crucial role in regulating neurotransmitters in the brain by facilitating their uptake and storage within vesicles, preparing them for exocytotic release. Because of its central role in neurotransmitter signalling and neuroprotection, VMAT2 is a target for neurodegenerative diseases and movement disorders, with its inhibitor being used as therapeutics. Despite the importance of VMAT2 in pharmacophysiology, the molecular basis of VMAT2-mediated neurotransmitter transport and its inhibition remains unclear. Here we show the cryo-electron microscopy structure of VMAT2 in the substrate-free state, in complex with the neurotransmitter dopamine, and in complex with the inhibitor tetrabenazine. In addition to these structural determinations, monoamine uptake assays, mutational studies, and pKa value predictions were performed to characterize the dynamic changes in VMAT2 structure. These results provide a structural basis for understanding VMAT2-mediated vesicular transport of neurotransmitters and a platform for modulation of current inhibitor design. en-copyright= kn-copyright= en-aut-name=ImDohyun en-aut-sei=Im en-aut-mei=Dohyun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=JormakkaMika en-aut-sei=Jormakka en-aut-mei=Mika kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=JugeNarinobu en-aut-sei=Juge en-aut-mei=Narinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KishikawaJun-ichi en-aut-sei=Kishikawa en-aut-mei=Jun-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KatoTakayuki en-aut-sei=Kato en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SugitaYukihiko en-aut-sei=Sugita en-aut-mei=Yukihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NodaTakeshi en-aut-sei=Noda en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UemuraTomoko en-aut-sei=Uemura en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=ShiimuraYuki en-aut-sei=Shiimura en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MiyajiTakaaki en-aut-sei=Miyaji en-aut-mei=Takaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=AsadaHidetsugu en-aut-sei=Asada en-aut-mei=Hidetsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=IwataSo en-aut-sei=Iwata en-aut-mei=So kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= affil-num=2 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= affil-num=3 en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University kn-affil= affil-num=4 en-affil=Department of Applied Biology, Kyoto Institute of Technology kn-affil= affil-num=5 en-affil=Institute for Protein Research, Osaka University kn-affil= affil-num=6 en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University kn-affil= affil-num=7 en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University kn-affil= affil-num=8 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= affil-num=9 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= affil-num=10 en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University kn-affil= affil-num=11 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= affil-num=12 en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7 article-no= start-page=002112 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250725 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses (ICTV) from the Animal dsRNA and ssRNA(?) Viruses Subcommittee, 2025 en-subtitle= kn-subtitle= en-abstract= kn-abstract=RNA viruses are ubiquitous in the environment and are important pathogens of humans, animals and plants. In 2024, the International Committee on Taxonomy of Viruses Animal dsRNA and ssRNA(?) Viruses Subcommittee submitted 18 taxonomic proposals for consideration. These proposals expanded the known virosphere by classifying 9 new genera and 88 species for newly detected virus genomes. Of note, newly established species expand the large family of Rhabdoviridae to 580 species. A new species in the family Arenaviridae includes a virus detected in Antarctic fish with a unique split nucleoprotein ORF. Additionally, four new species were established for historically isolated viruses with previously unsequenced genomes. Furthermore, three species were abolished due to incomplete genome sequence information, and one family was moved from being unassigned in the phylum Negarnaviricota into a subphylum and order. Herein, we summarize the 18 ratified taxonomic proposals and the general features of the current taxonomy, thereby supporting public and animal health responses. en-copyright= kn-copyright= en-aut-name=HughesHolly R. en-aut-sei=Hughes en-aut-mei=Holly R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=BallingerMatthew J. en-aut-sei=Ballinger en-aut-mei=Matthew J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=BaoYiming en-aut-sei=Bao en-aut-mei=Yiming kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=BejermanNicolas en-aut-sei=Bejerman en-aut-mei=Nicolas kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=BlasdellKim R. en-aut-sei=Blasdell en-aut-mei=Kim R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=BrieseThomas en-aut-sei=Briese en-aut-mei=Thomas kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=BrignoneJulia en-aut-sei=Brignone en-aut-mei=Julia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=CarreraJean Paul en-aut-sei=Carrera en-aut-mei=Jean Paul kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=De ConinckLander en-aut-sei=De Coninck en-aut-mei=Lander kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=de SouzaWilliam Marciel en-aut-sei=de Souza en-aut-mei=William Marciel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=DebatHumberto en-aut-sei=Debat en-aut-mei=Humberto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=DietzgenRalf G. en-aut-sei=Dietzgen en-aut-mei=Ralf G. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=D?rrwaldRalf en-aut-sei=D?rrwald en-aut-mei=Ralf kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=ErdinMert en-aut-sei=Erdin en-aut-mei=Mert kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=FooksAnthony R. en-aut-sei=Fooks en-aut-mei=Anthony R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=ForbesKristian M. en-aut-sei=Forbes en-aut-mei=Kristian M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=Freitas-Ast?aJuliana en-aut-sei=Freitas-Ast?a en-aut-mei=Juliana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=GarciaJorge B. en-aut-sei=Garcia en-aut-mei=Jorge B. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=GeogheganJemma L. en-aut-sei=Geoghegan en-aut-mei=Jemma L. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=GrimwoodRebecca M. en-aut-sei=Grimwood en-aut-mei=Rebecca M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=HorieMasayuki en-aut-sei=Horie en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=HyndmanTimothy H. en-aut-sei=Hyndman en-aut-mei=Timothy H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=JohneReimar en-aut-sei=Johne en-aut-mei=Reimar kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=KlenaJohn D. en-aut-sei=Klena en-aut-mei=John D. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= en-aut-name=KooninEugene V. en-aut-sei=Koonin en-aut-mei=Eugene V. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=26 ORCID= en-aut-name=KostygovAlexei Y. en-aut-sei=Kostygov en-aut-mei=Alexei Y. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=27 ORCID= en-aut-name=KrupovicMart en-aut-sei=Krupovic en-aut-mei=Mart kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=28 ORCID= en-aut-name=KuhnJens H. en-aut-sei=Kuhn en-aut-mei=Jens H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=29 ORCID= en-aut-name=LetkoMichael en-aut-sei=Letko en-aut-mei=Michael kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=30 ORCID= en-aut-name=LiJun-Min en-aut-sei=Li en-aut-mei=Jun-Min kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=31 ORCID= en-aut-name=LiuYiyun en-aut-sei=Liu en-aut-mei=Yiyun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=32 ORCID= en-aut-name=MartinMaria Laura en-aut-sei=Martin en-aut-mei=Maria Laura kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=33 ORCID= en-aut-name=MullNathaniel en-aut-sei=Mull en-aut-mei=Nathaniel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=34 ORCID= en-aut-name=NazarYael en-aut-sei=Nazar en-aut-mei=Yael kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=35 ORCID= en-aut-name=NowotnyNorbert en-aut-sei=Nowotny en-aut-mei=Norbert kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=36 ORCID= en-aut-name=NunesM?rcio Roberto Teixeira en-aut-sei=Nunes en-aut-mei=M?rcio Roberto Teixeira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=37 ORCID= en-aut-name=?klandArnfinn Lodden en-aut-sei=?kland en-aut-mei=Arnfinn Lodden kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=38 ORCID= en-aut-name=RubbenstrothDennis en-aut-sei=Rubbenstroth en-aut-mei=Dennis kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=39 ORCID= en-aut-name=RussellBrandy J. en-aut-sei=Russell en-aut-mei=Brandy J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=40 ORCID= en-aut-name=SchottEric en-aut-sei=Schott en-aut-mei=Eric kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=41 ORCID= en-aut-name=SeifertStephanie en-aut-sei=Seifert en-aut-mei=Stephanie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=42 ORCID= en-aut-name=SenCarina en-aut-sei=Sen en-aut-mei=Carina kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=43 ORCID= en-aut-name=ShedroffElizabeth en-aut-sei=Shedroff en-aut-mei=Elizabeth kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=44 ORCID= en-aut-name=SironenTarja en-aut-sei=Sironen en-aut-mei=Tarja kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=45 ORCID= en-aut-name=SmuraTeemu en-aut-sei=Smura en-aut-mei=Teemu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=46 ORCID= en-aut-name=TavaresCamila Prestes Dos Santos en-aut-sei=Tavares en-aut-mei=Camila Prestes Dos Santos kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=47 ORCID= en-aut-name=TeshRobert B. en-aut-sei=Tesh en-aut-mei=Robert B. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=48 ORCID= en-aut-name=TilstonNatasha L. en-aut-sei=Tilston en-aut-mei=Natasha L. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=49 ORCID= en-aut-name=TordoNo?l en-aut-sei=Tordo en-aut-mei=No?l kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=50 ORCID= en-aut-name=VasilakisNikos en-aut-sei=Vasilakis en-aut-mei=Nikos kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=51 ORCID= en-aut-name=WalkerPeter J. en-aut-sei=Walker en-aut-mei=Peter J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=52 ORCID= en-aut-name=WangFei en-aut-sei=Wang en-aut-mei=Fei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=53 ORCID= en-aut-name=WhitfieldAnna E. en-aut-sei=Whitfield en-aut-mei=Anna E. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=54 ORCID= en-aut-name=WhitmerShannon L.M. en-aut-sei=Whitmer en-aut-mei=Shannon L.M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=55 ORCID= en-aut-name=WolfYuri I. en-aut-sei=Wolf en-aut-mei=Yuri I. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=56 ORCID= en-aut-name=XiaHan en-aut-sei=Xia en-aut-mei=Han kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=57 ORCID= en-aut-name=YeGong-Yin en-aut-sei=Ye en-aut-mei=Gong-Yin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=58 ORCID= en-aut-name=YeZhuangxin en-aut-sei=Ye en-aut-mei=Zhuangxin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=59 ORCID= en-aut-name=YurchenkoVyacheslav en-aut-sei=Yurchenko en-aut-mei=Vyacheslav kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=60 ORCID= en-aut-name=ZhaoMingli en-aut-sei=Zhao en-aut-mei=Mingli kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=61 ORCID= affil-num=1 en-affil=Centers for Disease Control and Prevention kn-affil= affil-num=2 en-affil=Biological Sciences, Mississippi State University kn-affil= affil-num=3 en-affil=National Genomics Data Center, China National Center for Bioinformation; Beijing Institute of Genomics, Chinese Academy of Sciences; University of Chinese Academy of Sciences kn-affil= affil-num=4 en-affil=Consejo Nacional de Investigaciones Cient?ficas y T?cnicas (CONICET) and Instituto Nacional de Tecnolog?a Agropecuaria (INTA) kn-affil= affil-num=5 en-affil=CSIRO Health and Biosecurity kn-affil= affil-num=6 en-affil=Center for Infection and Immunity, and Department of Epidemiology, Mailman School of Public Health, Columbia University kn-affil= affil-num=7 en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS kn-affil= affil-num=8 en-affil=Instituto Conmemorativo Gorgas de Estudios de la Salud kn-affil= affil-num=9 en-affil=Division of Clinical and Epidemiological Virology, KU Leuven kn-affil= affil-num=10 en-affil=Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky kn-affil= affil-num=11 en-affil=Instituto Nacional de Tecnolog?a Agropecuaria (INTA) kn-affil= affil-num=12 en-affil=QAAFI, The University of Queensland kn-affil= affil-num=13 en-affil=Robert Koch Institut kn-affil= affil-num=14 en-affil=Department of Virology, University of Helsinki kn-affil= affil-num=15 en-affil=Animal and Plant Health Agency (APHA) kn-affil= affil-num=16 en-affil=Department of Biological Sciences, University of Arkansas kn-affil= affil-num=17 en-affil=Embrapa Cassava and Fruits kn-affil= affil-num=18 en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS kn-affil= affil-num=19 en-affil=Department of Microbiology and Immunology, University of Otago kn-affil= affil-num=20 en-affil=Department of Microbiology and Immunology, University of Otago kn-affil= affil-num=21 en-affil=Osaka International Research Center for Infectious Diseases, Osaka Metropolitan University kn-affil= affil-num=22 en-affil=School of Veterinary Medicine, Murdoch University kn-affil= affil-num=23 en-affil=German Federal Institute for Risk Assessment kn-affil= affil-num=24 en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention kn-affil= affil-num=25 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=26 en-affil=Computational Biology Branch, Division of Intramural Research National Library of Medicine, National Institutes of Health kn-affil= affil-num=27 en-affil=University of Ostrava kn-affil= affil-num=28 en-affil=Institut Pasteur, Universit? Paris Cit?, CNRS UMR6047, Archaeal Virology Unit kn-affil= affil-num=29 en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health kn-affil= affil-num=30 en-affil=Paul G. Allen School for Global Health, Washington State University kn-affil= affil-num=31 en-affil=Institute of Plant Virology, Ningbo University kn-affil= affil-num=32 en-affil=National Genomics Data Center, China National Center for Bioinformation; Beijing Institute of Genomics, Chinese Academy of Sciences; University of Chinese Academy of Sciences kn-affil= affil-num=33 en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS kn-affil= affil-num=34 en-affil=Department of Natural Sciences, Shawnee State University kn-affil= affil-num=35 en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS kn-affil= affil-num=36 en-affil=College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai Health kn-affil= affil-num=37 en-affil=Universidade Federal do Par? kn-affil= affil-num=38 en-affil=Pharmaq Analytiq kn-affil= affil-num=39 en-affil=Institute of Diagnostic Virology, Friedrich-Loeffler-Institut kn-affil= affil-num=40 en-affil=Centers for Disease Control and Prevention kn-affil= affil-num=41 en-affil=Institute of Marine and Environmental Technology, University of Maryland Center for Environmental Science kn-affil= affil-num=42 en-affil=Paul G. Allen School for Global Health, Washington State University kn-affil= affil-num=43 en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS kn-affil= affil-num=44 en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention kn-affil= affil-num=45 en-affil=Department of Virology, University of Helsinki kn-affil= affil-num=46 en-affil=Department of Virology, University of Helsinki kn-affil= affil-num=47 en-affil=Integrated Group of Aquaculture and Environmental Studies, Federal University of Paran? kn-affil= affil-num=48 en-affil=Department of Pathology, The University of Texas Medical Branch kn-affil= affil-num=49 en-affil=Department of Microbiology and Immunology, Indiana University School of Medicine kn-affil= affil-num=50 en-affil=Institut Pasteur kn-affil= affil-num=51 en-affil=Department of Pathology, The University of Texas Medical Branch kn-affil= affil-num=52 en-affil=University of Queensland kn-affil= affil-num=53 en-affil=Wuhan Institute of Virology, Chinese Academy of Sciences kn-affil= affil-num=54 en-affil=North Carolina State University kn-affil= affil-num=55 en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention kn-affil= affil-num=56 en-affil=Computational Biology Branch, Division of Intramural Research National Library of Medicine, National Institutes of Health kn-affil= affil-num=57 en-affil=Wuhan Institute of Virology, Chinese Academy of Sciences kn-affil= affil-num=58 en-affil=Institute of Insect Sciences, Zhejiang University kn-affil= affil-num=59 en-affil=Institute of Plant Virology, Ningbo University kn-affil= affil-num=60 en-affil=University of Ostrava kn-affil= affil-num=61 en-affil=Department of Pathobiology and Population Sciences, Royal Veterinary College kn-affil= END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7 article-no= start-page=002114 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250725 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses from the Plant Viruses Subcommittee, 2025 en-subtitle= kn-subtitle= en-abstract= kn-abstract=In March 2025, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote, newly proposed taxa were added to those under the mandate of the Plant Viruses Subcommittee. In brief, 1 new order, 3 new families, 6 new genera, 2 new subgenera and 206 new species were created. Some taxa were reorganized. Genus Cytorhabdovirus in the family Rhabdoviridae was abolished and its taxa were redistributed into three new genera Alphacytorhabdovirus, Betacytorhabdovirus and Gammacytorhabdovirus. Genus Waikavirus in the family Secoviridae was reorganized into two subgenera (Actinidivirus and Ritunrivirus). One family and four previously unaffiliated genera were moved to the newly established order Tombendovirales. Twelve species not assigned to a genus were abolished. To comply with the ICTV mandate of a binomial format for virus species, eight species were renamed. Demarcation criteria in the absence of biological information were defined in the genus Ilarvirus (family Bromoviridae). This article presents the updated taxonomy put forth by the Plant Viruses Subcommittee and ratified by the ICTV. en-copyright= kn-copyright= en-aut-name=RubinoLuisa en-aut-sei=Rubino en-aut-mei=Luisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AbrahamianPeter en-aut-sei=Abrahamian en-aut-mei=Peter kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AnWenxia en-aut-sei=An en-aut-mei=Wenxia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ArandaMiguel A. en-aut-sei=Aranda en-aut-mei=Miguel A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=Ascencio-Iba?ezJos? T. en-aut-sei=Ascencio-Iba?ez en-aut-mei=Jos? T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=BejermanNicolas en-aut-sei=Bejerman en-aut-mei=Nicolas kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=BlouinArnaud G. en-aut-sei=Blouin en-aut-mei=Arnaud G. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=CandresseThierry en-aut-sei=Candresse en-aut-mei=Thierry kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=CantoTomas en-aut-sei=Canto en-aut-mei=Tomas kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=CaoMengji en-aut-sei=Cao en-aut-mei=Mengji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=CarrJohn P. en-aut-sei=Carr en-aut-mei=John P. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=ChoWon Kyong en-aut-sei=Cho en-aut-mei=Won Kyong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=ConstableFiona en-aut-sei=Constable en-aut-mei=Fiona kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=DasguptaIndranil en-aut-sei=Dasgupta en-aut-mei=Indranil kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=DebatHumberto en-aut-sei=Debat en-aut-mei=Humberto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=DietzgenRalf G. en-aut-sei=Dietzgen en-aut-mei=Ralf G. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=DigiaroMichele en-aut-sei=Digiaro en-aut-mei=Michele kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=DonaireLivia en-aut-sei=Donaire en-aut-mei=Livia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=ElbeainoToufic en-aut-sei=Elbeaino en-aut-mei=Toufic kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=FargetteDenis en-aut-sei=Fargette en-aut-mei=Denis kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=FilardoFiona en-aut-sei=Filardo en-aut-mei=Fiona kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=FischerMatthias G. en-aut-sei=Fischer en-aut-mei=Matthias G. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=FontdevilaNuria en-aut-sei=Fontdevila en-aut-mei=Nuria kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=FoxAdrian en-aut-sei=Fox en-aut-mei=Adrian kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=Freitas-AstuaJuliana en-aut-sei=Freitas-Astua en-aut-mei=Juliana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= en-aut-name=FuchsMarc en-aut-sei=Fuchs en-aut-mei=Marc kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=26 ORCID= en-aut-name=GeeringAndrew D.W. en-aut-sei=Geering en-aut-mei=Andrew D.W. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=27 ORCID= en-aut-name=GhafariMahan en-aut-sei=Ghafari en-aut-mei=Mahan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=28 ORCID= en-aut-name=Hafr?nAnders en-aut-sei=Hafr?n en-aut-mei=Anders kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=29 ORCID= en-aut-name=HammondJohn en-aut-sei=Hammond en-aut-mei=John kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=30 ORCID= en-aut-name=HammondRosemarie en-aut-sei=Hammond en-aut-mei=Rosemarie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=31 ORCID= en-aut-name=Hasi?w-JaroszewskaBeata en-aut-sei=Hasi?w-Jaroszewska en-aut-mei=Beata kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=32 ORCID= en-aut-name=HebrardEugenie en-aut-sei=Hebrard en-aut-mei=Eugenie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=33 ORCID= en-aut-name=Hern?ndezCarmen en-aut-sei=Hern?ndez en-aut-mei=Carmen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=34 ORCID= en-aut-name=HilyJean-Michel en-aut-sei=Hily en-aut-mei=Jean-Michel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=35 ORCID= en-aut-name=HosseiniAhmed en-aut-sei=Hosseini en-aut-mei=Ahmed kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=36 ORCID= en-aut-name=HullRoger en-aut-sei=Hull en-aut-mei=Roger kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=37 ORCID= en-aut-name=Inoue-NagataAlice K. en-aut-sei=Inoue-Nagata en-aut-mei=Alice K. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=38 ORCID= en-aut-name=JordanRamon en-aut-sei=Jordan en-aut-mei=Ramon kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=39 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=40 ORCID= en-aut-name=KreuzeJan F. en-aut-sei=Kreuze en-aut-mei=Jan F. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=41 ORCID= en-aut-name=KrupovicMart en-aut-sei=Krupovic en-aut-mei=Mart kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=42 ORCID= en-aut-name=KubotaKenji en-aut-sei=Kubota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=43 ORCID= en-aut-name=KuhnJens H. en-aut-sei=Kuhn en-aut-mei=Jens H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=44 ORCID= en-aut-name=LeisnerScott en-aut-sei=Leisner en-aut-mei=Scott kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=45 ORCID= en-aut-name=LettJean-Michel en-aut-sei=Lett en-aut-mei=Jean-Michel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=46 ORCID= en-aut-name=LiChengyu en-aut-sei=Li en-aut-mei=Chengyu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=47 ORCID= en-aut-name=LiFan en-aut-sei=Li en-aut-mei=Fan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=48 ORCID= en-aut-name=LiJun Min en-aut-sei=Li en-aut-mei=Jun Min kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=49 ORCID= en-aut-name=L?pez-LambertiniPaola M. en-aut-sei=L?pez-Lambertini en-aut-mei=Paola M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=50 ORCID= en-aut-name=Lopez-MoyaJuan J. en-aut-sei=Lopez-Moya en-aut-mei=Juan J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=51 ORCID= en-aut-name=MaclotFrancois en-aut-sei=Maclot en-aut-mei=Francois kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=52 ORCID= en-aut-name=M?kinenKristiina en-aut-sei=M?kinen en-aut-mei=Kristiina kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=53 ORCID= en-aut-name=MartinDarren en-aut-sei=Martin en-aut-mei=Darren kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=54 ORCID= en-aut-name=MassartSebastien en-aut-sei=Massart en-aut-mei=Sebastien kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=55 ORCID= en-aut-name=MillerW. Allen en-aut-sei=Miller en-aut-mei=W. Allen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=56 ORCID= en-aut-name=MohammadiMusa en-aut-sei=Mohammadi en-aut-mei=Musa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=57 ORCID= en-aut-name=MollovDimitre en-aut-sei=Mollov en-aut-mei=Dimitre kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=58 ORCID= en-aut-name=MullerEmmanuelle en-aut-sei=Muller en-aut-mei=Emmanuelle kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=59 ORCID= en-aut-name=NagataTatsuya en-aut-sei=Nagata en-aut-mei=Tatsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=60 ORCID= en-aut-name=Navas-CastilloJes?s en-aut-sei=Navas-Castillo en-aut-mei=Jes?s kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=61 ORCID= en-aut-name=NeriyaYutaro en-aut-sei=Neriya en-aut-mei=Yutaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=62 ORCID= en-aut-name=Ochoa-CoronaFrancisco M. en-aut-sei=Ochoa-Corona en-aut-mei=Francisco M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=63 ORCID= en-aut-name=OhshimaKazusato en-aut-sei=Ohshima en-aut-mei=Kazusato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=64 ORCID= en-aut-name=Pall?sVicente en-aut-sei=Pall?s en-aut-mei=Vicente kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=65 ORCID= en-aut-name=PappuHanu en-aut-sei=Pappu en-aut-mei=Hanu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=66 ORCID= en-aut-name=PetrzikKarel en-aut-sei=Petrzik en-aut-mei=Karel kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=67 ORCID= en-aut-name=PoogginMikhail en-aut-sei=Pooggin en-aut-mei=Mikhail kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=68 ORCID= en-aut-name=PrigigalloMaria Isabella en-aut-sei=Prigigallo en-aut-mei=Maria Isabella kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=69 ORCID= en-aut-name=Ramos-Gonz?lezPedro L. en-aut-sei=Ramos-Gonz?lez en-aut-mei=Pedro L. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=70 ORCID= en-aut-name=RibeiroSimone en-aut-sei=Ribeiro en-aut-mei=Simone kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=71 ORCID= en-aut-name=Richert-P?ggelerKatja R. en-aut-sei=Richert-P?ggeler en-aut-mei=Katja R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=72 ORCID= en-aut-name=RoumagnacPhilippe en-aut-sei=Roumagnac en-aut-mei=Philippe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=73 ORCID= en-aut-name=RoyAvijit en-aut-sei=Roy en-aut-mei=Avijit kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=74 ORCID= en-aut-name=SabanadzovicSead en-aut-sei=Sabanadzovic en-aut-mei=Sead kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=75 ORCID= en-aut-name=?af??ov?Dana en-aut-sei=?af??ov? en-aut-mei=Dana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=76 ORCID= en-aut-name=SaldarelliPasquale en-aut-sei=Saldarelli en-aut-mei=Pasquale kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=77 ORCID= en-aut-name=Sanfa?onH?l?ne en-aut-sei=Sanfa?on en-aut-mei=H?l?ne kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=78 ORCID= en-aut-name=SarmientoCecilia en-aut-sei=Sarmiento en-aut-mei=Cecilia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=79 ORCID= en-aut-name=SasayaTakahide en-aut-sei=Sasaya en-aut-mei=Takahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=80 ORCID= en-aut-name=ScheetsKay en-aut-sei=Scheets en-aut-mei=Kay kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=81 ORCID= en-aut-name=SchravesandeWillem E.W. en-aut-sei=Schravesande en-aut-mei=Willem E.W. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=82 ORCID= en-aut-name=SealSusan en-aut-sei=Seal en-aut-mei=Susan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=83 ORCID= en-aut-name=ShimomotoYoshifumi en-aut-sei=Shimomoto en-aut-mei=Yoshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=84 ORCID= en-aut-name=S?meraMerike en-aut-sei=S?mera en-aut-mei=Merike kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=85 ORCID= en-aut-name=StavoloneLivia en-aut-sei=Stavolone en-aut-mei=Livia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=86 ORCID= en-aut-name=StewartLucy R. en-aut-sei=Stewart en-aut-mei=Lucy R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=87 ORCID= en-aut-name=TeycheneyPierre-Yves en-aut-sei=Teycheney en-aut-mei=Pierre-Yves kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=88 ORCID= en-aut-name=ThomasJohn E. en-aut-sei=Thomas en-aut-mei=John E. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=89 ORCID= en-aut-name=ThompsonJeremy R. en-aut-sei=Thompson en-aut-mei=Jeremy R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=90 ORCID= en-aut-name=TiberiniAntonio en-aut-sei=Tiberini en-aut-mei=Antonio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=91 ORCID= en-aut-name=TomitakaYasuhiro en-aut-sei=Tomitaka en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=92 ORCID= en-aut-name=TzanetakisIoannis en-aut-sei=Tzanetakis en-aut-mei=Ioannis kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=93 ORCID= en-aut-name=UmberMarie en-aut-sei=Umber en-aut-mei=Marie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=94 ORCID= en-aut-name=UrbinoCica en-aut-sei=Urbino en-aut-mei=Cica kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=95 ORCID= en-aut-name=van den BurgHarrold A. en-aut-sei=van den Burg en-aut-mei=Harrold A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=96 ORCID= en-aut-name=Van der VlugtRen? A.A. en-aut-sei=Van der Vlugt en-aut-mei=Ren? A.A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=97 ORCID= en-aut-name=VarsaniArvind en-aut-sei=Varsani en-aut-mei=Arvind kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=98 ORCID= en-aut-name=VerhageAdriaan en-aut-sei=Verhage en-aut-mei=Adriaan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=99 ORCID= en-aut-name=VillamorDan en-aut-sei=Villamor en-aut-mei=Dan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=100 ORCID= en-aut-name=von BargenSusanne en-aut-sei=von Bargen en-aut-mei=Susanne kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=101 ORCID= en-aut-name=WalkerPeter J. en-aut-sei=Walker en-aut-mei=Peter J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=102 ORCID= en-aut-name=WetzelThierry en-aut-sei=Wetzel en-aut-mei=Thierry kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=103 ORCID= en-aut-name=WhitfieldAnna E. en-aut-sei=Whitfield en-aut-mei=Anna E. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=104 ORCID= en-aut-name=WylieStephen J. en-aut-sei=Wylie en-aut-mei=Stephen J. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=105 ORCID= en-aut-name=YangCaixia en-aut-sei=Yang en-aut-mei=Caixia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=106 ORCID= en-aut-name=ZerbiniF. Murilo en-aut-sei=Zerbini en-aut-mei=F. Murilo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=107 ORCID= en-aut-name=ZhangSong en-aut-sei=Zhang en-aut-mei=Song kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=108 ORCID= affil-num=1 en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR kn-affil= affil-num=2 en-affil=USDA-ARS, BARC, National Germplasm Resources Laboratory kn-affil= affil-num=3 en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University kn-affil= affil-num=4 en-affil=Centro de Edafolog?a y Biolog?a Aplicada del Segura-CSIC kn-affil= affil-num=5 en-affil=Department of Molecular and Structural Biochemistry, North Carolina State University kn-affil= affil-num=6 en-affil=Unidad de Fitopatolog?a y Modelizaci?n Agr?cola (UFYMA) INTA-CONICET kn-affil= affil-num=7 en-affil=Plant Protection Department kn-affil= affil-num=8 en-affil=UMR 1332 Biologie du Fruit et Pathologie, University of Bordeaux, INRAE kn-affil= affil-num=9 en-affil=Margarita Salas Center for Biological Research (CIB-CSIC) Spanish Council for Scientific Research (CSIC) kn-affil= affil-num=10 en-affil=National Citrus Engineering and Technology Research Center, Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Citrus Research Institute, Southwest University kn-affil= affil-num=11 en-affil=Department of Plant Sciences, University of Cambridge kn-affil= affil-num=12 en-affil=Agriculture and Life Sciences Research Institute, Kangwon National University kn-affil= affil-num=13 en-affil=Agriculture Victoria Research, Department of Energy, Environment and Climate Action and School of Applied Systems Biology, La Trobe University kn-affil= affil-num=14 en-affil=University of Delhi South Campu kn-affil= affil-num=15 en-affil=Unidad de Fitopatolog?a y Modelizaci?n Agr?cola (UFYMA) INTA-CONICET kn-affil= affil-num=16 en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland kn-affil= affil-num=17 en-affil=CIHEAM, Istituto Agronomico Mediterraneo of Bari kn-affil= affil-num=18 en-affil=Centro de Edafolog?a y Biolog?a Aplicada del Segura-CSIC kn-affil= affil-num=19 en-affil=CIHEAM, Istituto Agronomico Mediterraneo of Bari kn-affil= affil-num=20 en-affil=Virus South Data kn-affil= affil-num=21 en-affil=Queensland Department of Primary Industries kn-affil= affil-num=22 en-affil=Max Planck Institute for Marine Microbiology kn-affil= affil-num=23 en-affil=Plant Protection Department kn-affil= affil-num=24 en-affil=Fera Science Ltd (Fera), York Biotech Campus kn-affil= affil-num=25 en-affil=Embrapa Cassava and Fruits, Brazilian Agricultural Research Corporation kn-affil= affil-num=26 en-affil=Plant Pathology, Cornell University kn-affil= affil-num=27 en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland kn-affil= affil-num=28 en-affil=Department of Biology, University of Oxford kn-affil= affil-num=29 en-affil=Swedish University of Agriculture kn-affil= affil-num=30 en-affil=USDA-ARS, USNA, Floral and Nursery Plants Research Unit kn-affil= affil-num=31 en-affil=USDA-ARS, BARC, Molecular Plant Pathology Laboratory kn-affil= affil-num=32 en-affil=Institute of Plant Protection-NRI kn-affil= affil-num=33 en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD, Institute Agro kn-affil= affil-num=34 en-affil=Instituto de Biolog?a Molecular y Celular de Plantas (IBMCP), Universitat Polit?cnica de Valencia-CSIC kn-affil= affil-num=35 en-affil=Institut Fran?ais de la Vigne et du Vin kn-affil= affil-num=36 en-affil=Vali-e-Asr University of Rafsanjan, Department of Plant Protection kn-affil= affil-num=37 en-affil=Retired from John Innes Centre kn-affil= affil-num=38 en-affil=Embrapa Hortali?as kn-affil= affil-num=39 en-affil=USDA-ARS, USNA, Floral and Nursery Plants Research Unit kn-affil= affil-num=40 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=41 en-affil=International Potato Center (CIP) kn-affil= affil-num=42 en-affil=Institut Pasteur, Universit? Paris Cit?, CNRS UMR6047, Archaeal Virology Unit kn-affil= affil-num=43 en-affil=Institute for Plant Protection, NARO kn-affil= affil-num=44 en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health kn-affil= affil-num=45 en-affil=Department of Biological Sciences, University of Toledo kn-affil= affil-num=46 en-affil=CIRAD, UMR PVBMT kn-affil= affil-num=47 en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University kn-affil= affil-num=48 en-affil=State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan Agricultural University kn-affil= affil-num=49 en-affil=Institute of Plant Virology, Ningbo University kn-affil= affil-num=50 en-affil=Instituto de Patolog?a Vegetal (IPAVE), INTA, Unidad de Fitopatolog?a y Modelizaci?n Agr?cola (UFYMA) INTA-CONICET kn-affil= affil-num=51 en-affil=Centre for Research in Agricultural Genomics, CRAG (CSIC-IRTA-UAB-UB) kn-affil= affil-num=52 en-affil=UMR 1332 Biologie du Fruit et Pathologie, University of Bordeaux, INRAE kn-affil= affil-num=53 en-affil=Department of Agricultural Sciences, University of Helsinki kn-affil= affil-num=54 en-affil=Institute of Infectious Disease and Molecular Medicine, University of Cape Town kn-affil= affil-num=55 en-affil=Plant Pathology Laboratory, TERRA Gembloux Agro-Bio Tech, University of Liege kn-affil= affil-num=56 en-affil=Department of Plant Pathology, Entomology and Microbiology, Iowa State University kn-affil= affil-num=57 en-affil=Department of Plant Protection, Gorgan University of Agricultural Sciences and Natural Resources kn-affil= affil-num=58 en-affil=USDA-APHIS, Plant Protection and Quarantine kn-affil= affil-num=59 en-affil=CIRAD, AGAP Institut; AGAP Institut, University of Montpellier; CIRAD, INRAE kn-affil= affil-num=60 en-affil=Instituto de Ci?ncias Biol?gicas, Universidade de Bras?lia kn-affil= affil-num=61 en-affil=Instituto de Hortofruticultura Subtropical y Mediterr?nea “La Mayora” (IHSM-UMA-CSIC), Consejo Superior de Investigaciones Cient?ficas kn-affil= affil-num=62 en-affil=Utsunomiya University kn-affil= affil-num=63 en-affil=Oklahoma State University, Institute for Biosecurity & Microbial Forensics kn-affil= affil-num=64 en-affil=Saga University kn-affil= affil-num=65 en-affil=Instituto de Biolog?a Molecular y Celular de Plantas (IBMCP), Universitat Polit?cnica de Valencia-CSIC kn-affil= affil-num=66 en-affil=Department of Plant Pathology, Washington State University kn-affil= affil-num=67 en-affil=Institute of Plant Molecular Biology kn-affil= affil-num=68 en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD kn-affil= affil-num=69 en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR kn-affil= affil-num=70 en-affil=Applied Molecular Biology Laboratory, Instituto Biol?gico de S?o Paulo kn-affil= affil-num=71 en-affil=Embrapa Recursos Gen?ticos e Biotecnologia kn-affil= affil-num=72 en-affil=Julius K?hn Institute, Federal Research Centre for Cultivated Plants, Institute for Epidemiology and Pathogen Diagnostics kn-affil= affil-num=73 en-affil=CIRAD, UMR PHIM kn-affil= affil-num=74 en-affil=USDA-ARS, BARC, Molecular Plant Pathology Laboratory, Beltsville, MD, USA kn-affil= affil-num=75 en-affil=Department of Agricultural Science and Plant Protection, Mississippi State University kn-affil= affil-num=76 en-affil=Department of Cell Biology and Genetics, Faculty of Science, Palack? University Olomouc kn-affil= affil-num=77 en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR kn-affil= affil-num=78 en-affil=Summerland Research and Development Centre, Agriculture and Agri-Food Canada kn-affil= affil-num=79 en-affil=Department of Chemistry and Biotechnology, Tallinn University of Technology kn-affil= affil-num=80 en-affil=Strategic Planning Headquarters, NARO kn-affil= affil-num=81 en-affil=Department of Plant Pathology, Ecology and Evolution, Oklahoma State University kn-affil= affil-num=82 en-affil=Molecular Plant Pathology, University of Amsterdam kn-affil= affil-num=83 en-affil=Natural Resources Institute, University of Greenwich kn-affil= affil-num=84 en-affil=Kochi Agricultural Research Center kn-affil= affil-num=85 en-affil=Department of Chemistry and Biotechnology, Tallinn University of Technology kn-affil= affil-num=86 en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR kn-affil= affil-num=87 en-affil=Currently unaffiliated kn-affil= affil-num=88 en-affil=CIRAD, UMR PVBMT & UMR PVBMT, Universit? de la R?union kn-affil= affil-num=89 en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland kn-affil= affil-num=90 en-affil=Plant Health and Environment Laboratory kn-affil= affil-num=91 en-affil=Council for Agricultural Research and Economics, Research Centre for Plant Protection and Certification kn-affil= affil-num=92 en-affil=Institute for Plant Protection, NARO kn-affil= affil-num=93 en-affil=Department of Entomology and Plant Pathology, Division of Agriculture, University of Arkansas System kn-affil= affil-num=94 en-affil=INRAE, UR ASTRO kn-affil= affil-num=95 en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD, Institute Agro kn-affil= affil-num=96 en-affil=Molecular Plant Pathology, University of Amsterdam kn-affil= affil-num=97 en-affil=Wageningen University and Research kn-affil= affil-num=98 en-affil=The Biodesign Center for Fundamental and Applied Microbiomics, Center for Evolution and Medicine, School of Life Sciences, Arizona State University kn-affil= affil-num=99 en-affil=Rijk Zwaan Breeding B.V. kn-affil= affil-num=100 en-affil=Department of Entomology and Plant Pathology, Division of Agriculture, University of Arkansas System kn-affil= affil-num=101 en-affil=Humboldt-Universit?t zu Berlin, Thaer-Institute of Agricultural and Horticultural Sciences kn-affil= affil-num=102 en-affil=The University of Queensland kn-affil= affil-num=103 en-affil=Dienstleistungszentrum L?ndlicher Raum Rheinpfalz kn-affil= affil-num=104 en-affil=North Carolina State University kn-affil= affil-num=105 en-affil=Food Futures Institute, Murdoch University kn-affil= affil-num=106 en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University kn-affil= affil-num=107 en-affil=Dep. de Fitopatologia/BIOAGRO, Universidade Federal de Vi?osa kn-affil= affil-num=108 en-affil=National Citrus Engineering and Technology Research Center, Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Citrus Research Institute, Southwest University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=3 article-no= start-page=104810 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=202503 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=An ultra-simplified protocol for PCR template preparation from both unsporulated and sporulated Eimeria oocysts en-subtitle= kn-subtitle= en-abstract= kn-abstract=Molecular biological techniques have enabled the accurate identification of the avian Eimeria parasite, however, the preparation of PCR template remains a bottleneck due to contaminants from feces and the robust oocyst's wall resistant to chemical and mechanical force. Generally, the preparation of PCR template involves three main steps: (1) pretreatment of oocysts; (2) disruption of oocysts; and (3) purification of genomic DNA. We prepared PCR templates from both unsporulated and sporulated E. tenella oocysts using various protocols, followed by species-specific PCR to define the limit of detection. Our data revealed that whereas neither pretreatment of oocysts with sodium hypochlorite nor purification of genomic DNA with commercial kits improved the limit of detection of PCR, disruption of oocysts was a critical step in the preparation of PCR templates. The most sensitive PCR assay was achieved with the template prepared by disrupting oocysts suspended in distilled water, followed by bead-beating and heating at 99°C for 5 min, which detected 0.16 oocysts per PCR. This ultra-simplified protocol for preparation of PCR template, which does not require expensive reagents or equipment, will significantly enhance the sensitive and efficient molecular identification of Eimeria. It will improve our understanding of the prevalence of this parasite at the species level and contribute to the development of techniques for the control in the field. en-copyright= kn-copyright= en-aut-name=TakanoAruto en-aut-sei=Takano en-aut-mei=Aruto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UmaliDennis V. en-aut-sei=Umali en-aut-mei=Dennis V. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=WardhanaApril H. en-aut-sei=Wardhana en-aut-mei=April H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SawitriDyah H. en-aut-sei=Sawitri en-aut-mei=Dyah H. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TeramotoIsao en-aut-sei=Teramoto en-aut-mei=Isao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HatabuToshimitsu en-aut-sei=Hatabu en-aut-mei=Toshimitsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KidoYasutoshi en-aut-sei=Kido en-aut-mei=Yasutoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KanekoAkira en-aut-sei=Kaneko en-aut-mei=Akira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SasaiKazumi en-aut-sei=Sasai en-aut-mei=Kazumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KatohHiromitsu en-aut-sei=Katoh en-aut-mei=Hiromitsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MatsubayashiMakoto en-aut-sei=Matsubayashi en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Departments of Veterinary Immunology, Graduate School of Veterinary Medical Sciences, Osaka Metropolitan University kn-affil= affil-num=2 en-affil=Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of the Philippines Los Ba?os, College kn-affil= affil-num=3 en-affil=Research Center for Veterinary Science, National Research and Innovation Agency kn-affil= affil-num=4 en-affil=Research Center for Veterinary Science, National Research and Innovation Agency kn-affil= affil-num=5 en-affil=Departments of Virology and Parasitology, Graduate School of Medicine, Osaka Metropolitan University kn-affil= affil-num=6 en-affil=Laboratory of Animal Physiology, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University kn-affil= affil-num=7 en-affil=Departments of Virology and Parasitology, Graduate School of Medicine, Osaka Metropolitan University kn-affil= affil-num=8 en-affil=Departments of Virology and Parasitology, Graduate School of Medicine, Osaka Metropolitan University kn-affil= affil-num=9 en-affil=Departments of Veterinary Immunology, Graduate School of Veterinary Medical Sciences, Osaka Metropolitan University kn-affil= affil-num=10 en-affil=Departments of Veterinary Immunology, Graduate School of Veterinary Medical Sciences, Osaka Metropolitan University kn-affil= affil-num=11 en-affil=Departments of Veterinary Immunology, Graduate School of Veterinary Medical Sciences, Osaka Metropolitan University kn-affil= en-keyword=Coccidian parasite kn-keyword=Coccidian parasite en-keyword=Eimeria tenella kn-keyword=Eimeria tenella en-keyword=Extraction kn-keyword=Extraction en-keyword=Molecular identification kn-keyword=Molecular identification en-keyword=Oocyst kn-keyword=Oocyst END start-ver=1.4 cd-journal=joma no-vol=99 cd-vols= no-issue=3 article-no= start-page=e02166-24 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2025 dt-pub=20250213 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A capsidless (+)RNA yadokarivirus hosted by a dsRNA virus is infectious as particles, cDNA, and dsRNA en-subtitle= kn-subtitle= en-abstract= kn-abstract=Capsidless yadokariviruses (members of the order Yadokarivirales) with (+)RNA genomes divert the capsid of their partner icosahedral double-stranded RNA (dsRNA) viruses in different families of the order Ghabrivirales into the replication site. A yadokarivirus, AfSV2, has been reported from a German strain of the ascomycete fungus Aspergillus foetidus coinfected by two dsRNA viruses, a victorivirus (AfSV1, family Pseudototiviridae) and an alternavirus (AfFV, family Alternaviridae). Here, we identified AfSV1 as the partner of AfSV2 in a Japanese A. foetidus strain after showing the infectiousness of AfSV2 in three forms: virus particles (heterocapsid), transforming full-length complementary DNA (cDNA), and purified replicated form (RF) dsRNA that is believed to be inactive as a translational template. Virion transfection of virus-free A. foetidus protoplasts resulted in the generation of two strains infected either by AfSV1 alone or by both AfSV1 and AfSV2. Transformants with AfSV2 full-length cDNA launched AfSV2 infection only in the presence of AfSV1, but not those with AfSV2 RNA-directed RNA polymerase mutant cDNA. The purified fractions containing AfSV2 RF dsRNA also launched infection when transfected into protoplasts infected by AfSV1. Treatment with dsRNA-specific RNase III, but not with proteinase K, S1 nuclease, or DNase I, abolished the infectivity of AfSV2 RF dsRNA. Furthermore, we confirmed the infectiousness of gel-purified AfSV2 RF dsRNA in the presence of AfSV1. Taken together, our results show the unique infectious entity of AfSV2 and the expansion of yadokarivirus partners in the family Pseudototiviridae and provide interesting evolutionary insights. en-copyright= kn-copyright= en-aut-name=FadliMuhammad en-aut-sei=Fadli en-aut-mei=Muhammad kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HisanoSakae en-aut-sei=Hisano en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NovoaGuy en-aut-sei=Novoa en-aut-mei=Guy kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Cast?nJos? R. en-aut-sei=Cast?n en-aut-mei=Jos? R. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Department of Structure of Macromolecules, Centro Nacional Biotecnolog?a (CNB-CSIC), Campus de Cantoblanco kn-affil= affil-num=4 en-affil=Department of Structure of Macromolecules, Centro Nacional Biotecnolog?a (CNB-CSIC), Campus de Cantoblanco kn-affil= affil-num=5 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=6 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= en-keyword=yadokarivirus kn-keyword=yadokarivirus en-keyword=hetero-encapsidation kn-keyword=hetero-encapsidation en-keyword=partner dsRNA virus kn-keyword=partner dsRNA virus en-keyword=fungal virus kn-keyword=fungal virus en-keyword=Aspergillus foetidus kn-keyword=Aspergillus foetidus en-keyword=neo-lifestyle kn-keyword=neo-lifestyle END start-ver=1.4 cd-journal=joma no-vol=10 cd-vols= no-issue=11 article-no= start-page=e31872 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2024 dt-pub=20240615 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Bacterial DNA and serum IgG antibody titer assays for assessing infection of human-pathogenic and dog-pathogenic Porphyromonas species in dogs en-subtitle= kn-subtitle= en-abstract= kn-abstract=Periodontal disease is highly prevalent in both humans and dogs. Although there have been reports of cross-infection of periodontopathic bacteria, methods for assessing it have yet to be established. The actual status of cross-infection remains to be seen. The purpose of this study was to evaluate the utility of bacterial DNA and serum immunoglobulin G (IgG) antibody titer assays to assess infection of human-pathogenic and dog-pathogenic Porphyromonas species in dogs. Four experimental beagles were used for establishing methods. Sixty-six companion dogs at veterinary clinics visiting for treatment and prophylaxis of periodontal disease were used and divided into healthy, gingivitis, and periodontitis groups. Periodontal pathogens such as Porphyromonas gingivalis and Porphyromonas gulae were investigated as target bacteria. DNA levels of both bacteria were measured using species-specific primers designed for real-time polymerase chain reaction (PCR). Serum IgG titers of both bacteria were measured by enzyme-linked immunosorbent assay (ELISA).
PCR primers were confirmed to have high sensitivity and specificity. However, there was no relationship between the amount of bacterial DNA and the severity of the periodontal disease. In addition, dogs with periodontitis had higher IgG titers against both bacteria compared to dogs in the healthy and gingivitis groups; there was cross-reactivity between the two bacteria. Receiver operating characteristic (ROC) analysis of IgG titers against both bacteria showed high sensitivity (>90 %) and specificity (>75 %). Since both bacteria were distinguished by DNA assays, the combination of these assays may be useful in the evaluation of cross-infection. en-copyright= kn-copyright= en-aut-name=Tai-TokuzenMasako en-aut-sei=Tai-Tokuzen en-aut-mei=Masako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ItoTakashi en-aut-sei=Ito en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TamuraKazuya en-aut-sei=Tamura en-aut-mei=Kazuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HirayamaHaruko en-aut-sei=Hirayama en-aut-mei=Haruko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NakamuraShin en-aut-sei=Nakamura en-aut-mei=Shin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OkuboKeisuke en-aut-sei=Okubo en-aut-mei=Keisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OmoriKazuhiro en-aut-sei=Omori en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YamamotoTadashi en-aut-sei=Yamamoto en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MominokiKatsumi en-aut-sei=Mominoki en-aut-mei=Katsumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Department of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital kn-affil= affil-num=2 en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Animal Resources, Advanced Science Research Center, Okayama University kn-affil= affil-num=5 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Center for Collaborative Research, Department of Oral Science and Translational Research, Nova Southeastern University kn-affil= affil-num=7 en-affil=Department of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital kn-affil= affil-num=8 en-affil=Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Comprehensive Dentistry, The Center for Graduate Medical Education (Dental Division), Okayama University Hospital kn-affil= affil-num=10 en-affil=Department of Animal Resources, Advanced Science Research Center, Okayama University kn-affil= affil-num=11 en-affil=Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Cross infection kn-keyword=Cross infection en-keyword=Human and dog kn-keyword=Human and dog en-keyword=Periodontal disease kn-keyword=Periodontal disease en-keyword=Porphyromonas gingivalis kn-keyword=Porphyromonas gingivalis en-keyword=Porphyromonas gulae kn-keyword=Porphyromonas gulae en-keyword=Detection assay kn-keyword=Detection assay END start-ver=1.4 cd-journal=joma no-vol=25 cd-vols= no-issue=6 article-no= start-page=3523 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2024 dt-pub=20240320 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Suppression of Borna Disease Virus Replication during Its Persistent Infection Using the CRISPR/Cas13b System en-subtitle= kn-subtitle= en-abstract= kn-abstract=Borna disease virus (BoDV-1) is a bornavirus that infects the central nervous systems of various animal species, including humans, and causes fatal encephalitis. BoDV-1 also establishes persistent infection in neuronal cells and causes neurobehavioral abnormalities. Once neuronal cells or normal neural networks are lost by BoDV-1 infection, it is difficult to regenerate damaged neural networks. Therefore, the development of efficient anti-BoDV-1 treatments is important to improve the outcomes of the infection. Recently, one of the clustered regularly interspaced short palindromic repeats (CRISPRs) and CRISPR-associated (Cas) systems, CRISPR/Cas13, has been utilized as antiviral tools. However, it is still unrevealed whether the CRISPR/Cas13 system can suppress RNA viruses in persistently infected cells. In this study, we addressed this question using persistently BoDV-1-infected cells. The CRISPR/Cas13 system targeting viral mRNAs efficiently decreased the levels of target viral mRNAs and genomic RNA (gRNA) in persistently infected cells. Furthermore, the CRISPR/Cas13 system targeting viral mRNAs also suppressed BoDV-1 infection if the system was introduced prior to the infection. Collectively, we demonstrated that the CRISPR/Cas13 system can suppress BoDV-1 in both acute and persistent infections. Our findings will open the avenue to treat prolonged infection with RNA viruses using the CRISPR/Cas13 system. en-copyright= kn-copyright= en-aut-name=SasakiShigenori en-aut-sei=Sasaki en-aut-mei=Shigenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KatohHirokazu en-aut-sei=Katoh en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=antiviral kn-keyword=antiviral en-keyword=antivirals kn-keyword=antivirals en-keyword=Borna disease virus kn-keyword=Borna disease virus en-keyword=CRISPR/Cas13b kn-keyword=CRISPR/Cas13b en-keyword=persistent infection kn-keyword=persistent infection END start-ver=1.4 cd-journal=joma no-vol=75 cd-vols= no-issue= article-no= start-page=102337 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=202310 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Continued mycovirus discovery expanding our understanding of virus lifestyles, symptom expression, and host defense en-subtitle= kn-subtitle= en-abstract= kn-abstract=High-throughput sequencing technologies have greatly expanded the RNA virome in general and have led to an exponential increase in new fungal viruses, also known as mycoviruses. Mycoviruses are omnipresent in fungi and usually induce symptomless infections. Some mycoviruses infecting fungi pathogenic to plants, insects, and mammals are known to modify host virulence positively and negatively and attract particular interests. In addition, fungal viruses continue to provide intriguing research materials and themes that lead to discoveries of peculiar viruses as infectious entities and insights into virus evolution and diversity. In this review, we outline the diversity and neolifestyle of recently discovered fungal RNA viruses, and phenotypic alterations induced by them. Furthermore, we discuss recent advances in research regarding the fungal antiviral defense and viral counterdefense, which are closely associated with host phenotype alterations. We hope that this article will enhance understanding of the interesting and growing fungal virology field. en-copyright= kn-copyright= en-aut-name=SatoYukiyo en-aut-sei=Sato en-aut-mei=Yukiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil=Institute for Plant Sciences, University of Cologne kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=13 cd-vols= no-issue=12 article-no= start-page=1706 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=20231124 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Roles of Human Endogenous Retroviruses and Endogenous Virus-Like Elements in Cancer Development and Innate Immunity en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections in the host genome. Although mutations and silencing mechanisms impair their original role in viral replication, HERVs are believed to play roles in various biological processes. Long interspersed nuclear elements (LINEs) are non-LTR retrotransposons that have a lifecycle resembling that of retroviruses. Although LINE expression is typically silenced in somatic cells, it also contributes to various biological processes. The aberrant expression of HERVs and LINEs is closely associated with the development of cancer and/or immunological diseases, suggesting that they are integrated into various pathways related to the diseases. HERVs/LINEs control gene expression depending on the context as promoter/enhancer elements. Some RNAs and proteins derived from HERVs/LINEs have oncogenic potential, whereas others stimulate innate immunity. Non-retroviral endogenous viral elements (nrEVEs) are a novel type of virus-like element in the genome. nrEVEs may also be involved in host immunity. This article provides a current understanding of how these elements impact cellular physiology in cancer development and innate immunity, and provides perspectives for future studies. en-copyright= kn-copyright= en-aut-name=KatohHirokazu en-aut-sei=Katoh en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=HERVs kn-keyword=HERVs en-keyword=LINEs kn-keyword=LINEs en-keyword=cancer kn-keyword=cancer en-keyword=innate immunity kn-keyword=innate immunity en-keyword=promoter kn-keyword=promoter en-keyword=enhancer kn-keyword=enhancer en-keyword=interferon signaling kn-keyword=interferon signaling END start-ver=1.4 cd-journal=joma no-vol=17 cd-vols= no-issue=1 article-no= start-page=65 end-page=72 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220130 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=COVID-19 and Spanish Flu, the Representative Pandemics of the 21st and 20th Centuries en-subtitle= kn-subtitle= en-abstract= kn-abstract=We are still in the early stage of 21st century and the two pandemics Spanish flu and COVID-19 are the presentative pandemics in 20th and 21st centuries, respectively. The Spanish flu pandemic raged from 1918 to 1920, just after World War I. It was the first influenza pandemic worldwide; since then, humankind has experienced many such pandemics. Spanish flu is caused by a virus. However, since virology was not well established at that time, the new clinical system was needed to cope with “unknown pathogen”; during the pandemic, high infection rates were recorded, but our predecessors managed to somehow tackle the situation. With respect to the ongoing COVID-19 pandemic, both the virus and its genome were clarified quickly. Nonetheless, it has turned out to be quite an intriguing infectious disease, with the high rates in developed countries, such as the US and those in Europe, which have aging societies, and low rates in developing countries such as those in Africa, where the population is largely young. Here, I compared and discuss the two pandemics, COVID-19 and Spanish flu. en-copyright= kn-copyright= en-aut-name=ShinodaSumio en-aut-sei=Shinoda en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil=Collaborative Research Center for Infectious Diseases in India, Okayama University kn-affil= en-keyword=COVID-19 kn-keyword=COVID-19 en-keyword=SARS-CoV-2 kn-keyword=SARS-CoV-2 en-keyword=vaccine kn-keyword=vaccine en-keyword=Spanish flu kn-keyword=Spanish flu en-keyword=influenza kn-keyword=influenza END start-ver=1.4 cd-journal=joma no-vol=167 cd-vols= no-issue=12 article-no= start-page=2833 end-page=2838 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20221022 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Identification of novel totiviruses from the ascomycetous fungus Geotrichum candidum en-subtitle= kn-subtitle= en-abstract= kn-abstract=Mycoviruses are widely distributed across the kingdom Fungi, including ascomycetous yeast strains of the class Saccharomycetes. Geotrichum candidum is an important fungal pathogen belonging to Saccharomycetes and has a diverse host range. Here, we report the characterization of four new classical totiviruses from two distinct Geotrichum candidum strains from Pakistan. The four identified viruses were tentatively named “Geotrichum candidum totivirus 1, 2, 3a, and 3b” (GcTV1-3b). The complete dsRNA genomes of the identified totiviruses are 4621, 4592, 4576, and 4576 bp in length, respectively. All totivirus genomes have two open reading frames, encoding a capsid protein (CP) and an RNA-dependent RNA polymerase (RdRP), respectively. The downstream RdRP domain is assumed to be expressed as a CP-RdRP fusion product via -1 frameshifting mediated by a heptameric slippery site. Sequence comparisons and phylogenetic analysis showed that each of the discovered viruses belongs to a new species of the genus Totivirus in the family Totiviridae, with GcTV1 and GcTV3 (a and b strains) clustering in one subgroup and GcTV2 in another subgroup. en-copyright= kn-copyright= en-aut-name=KhanHaris Ahmed en-aut-sei=Khan en-aut-mei=Haris Ahmed kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShahiSabitree en-aut-sei=Shahi en-aut-mei=Sabitree kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=BhattiMuhammad Faraz en-aut-sei=Bhatti en-aut-mei=Muhammad Faraz kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=4 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=15 cd-vols= no-issue=4 article-no= start-page=942 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=20230410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Impact of Borna Disease Virus Infection on the Transcriptome of Differentiated Neuronal Cells and Its Modulation by Antiviral Treatment en-subtitle= kn-subtitle= en-abstract= kn-abstract=Borna disease virus (BoDV-1) is a highly neurotropic RNA virus that causes neurobehavioral disturbances such as abnormal social activities and memory impairment. Although impairments in the neural circuits caused by BoDV-1 infection induce these disturbances, the molecular basis remains unclear. Furthermore, it is unknown whether anti-BoDV-1 treatments can attenuate BoDV-1-mediated transcriptomic changes in neuronal cells. In this study, we investigated the effects of BoDV-1 infection on neuronal differentiation and the transcriptome of differentiated neuronal cells using persistently BoDV-1-infected cells. Although BoDV-1 infection did not have a detectable effect on intracellular neuronal differentiation processes, differentiated neuronal cells exhibited transcriptomic changes in differentiation-related genes. Some of these transcriptomic changes, such as the decrease in the expression of apoptosis-related genes, were recovered by anti-BoDV-1 treatment, while alterations in the expression of other genes remained after treatment. We further demonstrated that a decrease in cell viability induced by differentiation processes in BoDV-1-infected cells can be relieved with anti-BoDV-1 treatment. This study provides fundamental information regarding transcriptomic changes after BoDV-1 infection and the treatment in neuronal cells. en-copyright= kn-copyright= en-aut-name=TengDa en-aut-sei=Teng en-aut-mei=Da kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UedaKeiji en-aut-sei=Ueda en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil=Division of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine kn-affil= affil-num=2 en-affil=Division of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine kn-affil= affil-num=3 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=antiviral kn-keyword=antiviral en-keyword=Borna disease virus kn-keyword=Borna disease virus en-keyword=neuronal cells kn-keyword=neuronal cells en-keyword=gene expression kn-keyword=gene expression en-keyword=differentiation kn-keyword=differentiation END start-ver=1.4 cd-journal=joma no-vol=134 cd-vols= no-issue=1 article-no= start-page=10 end-page=15 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Viral pathogenesis and the symbiosis between viruses and hosts kn-title=ウイルスと宿主との共生から見るウイルス病原性 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name=本田知之 kn-aut-sei=本田 kn-aut-mei=知之 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学学術研究院医歯薬学域　病原ウイルス学 en-keyword= ウイルス kn-keyword= ウイルス en-keyword=宿主 kn-keyword=宿主 en-keyword=共生 kn-keyword=共生 en-keyword=病原性 kn-keyword=病原性 en-keyword=免疫 kn-keyword=免疫 END start-ver=1.4 cd-journal=joma no-vol=76 cd-vols= no-issue=5 article-no= start-page=503 end-page=510 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=202210 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Viral Sequences Are Repurposed for Controlling Antiviral Responses as Non-Retroviral Endogenous Viral Elements en-subtitle= kn-subtitle= en-abstract= kn-abstract=Eukaryotic genomes contain numerous copies of endogenous viral elements (EVEs), most of which are considered endogenous retrovirus (ERV) sequences. Over the past decade, non-retroviral endogenous viral elements (nrEVEs) derived from ancient RNA viruses have been discovered. Several functions have been proposed for these elements, including antiviral defense. This review summarizes the current understanding of nrEVEs derived from RNA viruses, particularly endogenous bornavirus-like elements (EBLs) and endogenous filovirus-like elements (EFLs). EBLs are one of the most extensively studied nrEVEs. The EBL derived from bornavirus nucleoprotein (EBLN) is thought to function as a non-coding RNA or protein that regulates host gene expression or inhibits virus propagation. Ebolavirus and marburgvirus, which are filoviruses, induce severe hemorrhagic fever in humans and nonhuman primates. Although the ecology of filoviruses remains unclear, bats are believed to be potential reservoirs. Based on the knowledge from EBLs, it is postulated that EFLs in the bat genome help to maintain the balance between filovirus infection and the bat’s defense system, which may partially explain why bats act as potential reservoirs. Further research into the functions of nrEVEs could reveal novel antiviral systems and inspire novel antiviral approaches. en-copyright= kn-copyright= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=EVE kn-keyword=EVE en-keyword=nrEVE kn-keyword=nrEVE en-keyword=bornavirus kn-keyword=bornavirus en-keyword=filovirus kn-keyword=filovirus en-keyword=antiviral kn-keyword=antiviral END start-ver=1.4 cd-journal=joma no-vol=167 cd-vols= no-issue=4 article-no= start-page=1201 end-page=1204 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=202234 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A novel deltapartitivirus from red clover en-subtitle= kn-subtitle= en-abstract= kn-abstract=The family Partitiviridae has five genera, among which is the genus Deltapartitivirus. We report here the complete genome sequence of a deltapartitivirus from red clover, termed “red clover cryptic virus 3” (RCCV3). RCCV3 has a bisegmented double-stranded (ds) RNA genome. dsRNA1 and dsRNA2 are 1580 and 1589 nucleotides (nt) in length and are predicted to encode an RNA-directed RNA polymerase (RdRP) and a capsid protein (CP), respectively. The RCCV3 RdRP shares the highest sequence identity with the RdRP of a previously reported deltapartitivirus, Medicago sativa deltapartitivirus 1 (MsDPV1) (76.5%), while the RCCV3 CP shows 50% sequence identity to the CP of MsDPV1. RdRP- and CP-based phylogenetic trees place RCCV3 into a clade of deltapartitiviruses. The sequence and phylogenetic analyses clearly indicate that RCCV3 represents a new species in the genus Deltapartitivirus. RCCV3 was detectable in all three tested cultivars of red clover. en-copyright= kn-copyright= en-aut-name=TelengechPaul en-aut-sei=Telengech en-aut-mei=Paul kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShahiSabitree en-aut-sei=Shahi en-aut-mei=Sabitree kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=167 cd-vols= no-issue= article-no= start-page=923 end-page=929 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220203 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A novel victorivirus from the phytopathogenic fungus Neofusicoccum parvum en-subtitle= kn-subtitle= en-abstract= kn-abstract=Neofusicoccum parvum is an important plant-pathogenic ascomycetous fungus that causes trunk diseases in a variety of plants. A limited number of reports on mycoviruses from this fungus are available. Here, we report the characterization of a novel victorivirus, Neofusicoccum parvum victorivirus 3 (NpVV3). An agarose gel dsRNA profile of a Pakistani strain of N. parvum, NFN, showed a band of similar to 5 kbp that was not detectable in Japanese strains of N. parvum. Taking a high-throughput and Sanger sequencing approach, the complete genome sequence of NpVV3 was determined to be 5226 bp in length with two open reading frames (ORF1 and ORF2) that encode a capsid protein (CP) and an RNA-dependent RNA polymerase (RdRP). The RdRP appears to be translated by a stop/restart mechanism facilitated by the junction sequence AUGucUGA, as is found in some other victoriviruses. BLASTp searches showed that NpVV3 CP and RdRP share the highest amino acid sequence identity (80.5% and 72.4%, respectively) with the corresponding proteins of NpVV1 isolated from a French strain of N. parvum. However, NpVV3 was found to be different from NpVV1 in its terminal sequences and the stop/restart facilitator sequence. NpVV3 particles similar to 35 nm in diameter were partially purified and used to infect an antiviral-RNA-silencing-deficient strain (Delta cl2) of an experimental ascomycetous fungal host, Cryphonectria parasitica. NpVV3 showed symptomless infection in the new host strain. en-copyright= kn-copyright= en-aut-name=KhanHaris Ahmed en-aut-sei=Khan en-aut-mei=Haris Ahmed kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SatoYukiyo en-aut-sei=Sato en-aut-mei=Yukiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=JamalAtif en-aut-sei=Jamal en-aut-mei=Atif kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=BhattiMuhammad Faraz en-aut-sei=Bhatti en-aut-mei=Muhammad Faraz kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Crop Diseases Research Institute, National Agricultural Research Centre kn-affil= affil-num=5 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue=1 article-no= start-page=160 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220116 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Nectin-2 Acts as a Viral Entry Mediated Molecule That Binds to Human Herpesvirus 6B Glycoprotein B en-subtitle= kn-subtitle= en-abstract= kn-abstract=Human herpesvirus 6B (HHV-6B) is a T-lymphotropic virus and the etiological agent of exanthem subitum. HHV-6B is present in a latent or persistent form after primary infection and is produced in the salivary glands or transmitted to this organ. Infected individuals continue to secrete the virus in their saliva, which is thus considered a source for virus transmission. HHV-6B primarily propagates in T cells because its entry receptor, CD134, is mainly expressed by activated T cells. The virus then spreads to the host's organs, including the salivary glands, nervous system, and liver. However, CD134 expression is not detected in these organs. Therefore, HHV-6B may be entering cells via a currently unidentified cell surface molecule, but the mechanisms for this have not yet been investigated. In this study, we investigated a CD134-independent virus entry mechanism in the parotid-derived cell line HSY. First, we confirmed viral infection in CD134-membrane unanchored HSY cells. We then determined that nectin cell adhesion molecule 2 (nectin-2) mediated virus entry and that HHV-6B-insensitive T-cells transduced with nectin-2 were transformed into virus-permissive cells. We also found that virus entry was significantly reduced in nectin-2 knockout parotid-derived cells. Furthermore, we showed that HHV-6B glycoprotein B (gB) interacted with the nectin-2 V-set domain. The results suggest that nectin-2 acts as an HHV-6B entry-mediated protein. en-copyright= kn-copyright= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FujikuraDaisuke en-aut-sei=Fujikura en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NambaHikaru en-aut-sei=Namba en-aut-mei=Hikaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=School of Veterinary Medicine, Kitasato University kn-affil= affil-num=3 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=HHV-6B kn-keyword=HHV-6B en-keyword=nectin-2 kn-keyword=nectin-2 en-keyword=CD112 kn-keyword=CD112 en-keyword=CD134 kn-keyword=CD134 en-keyword=virus entry kn-keyword=virus entry en-keyword=glycoprotein B kn-keyword=glycoprotein B END start-ver=1.4 cd-journal=joma no-vol=88 cd-vols= no-issue=2 article-no= start-page=105 end-page=127 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220117 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Plant viruses and viroids in Japan en-subtitle= kn-subtitle= en-abstract= kn-abstract=An increasing number of plant viruses and viroids have been reported from all over the world due largely to metavirogenomics approaches with technological innovation. Herein, the official changes of virus taxonomy, including the establishment of megataxonomy and amendments of the codes of virus classification and nomenclature, recently made by the International Committee on Taxonomy of Viruses were summarized. The continued efforts of the plant virology community of Japan to index all plant viruses and viroids occurring in Japan, which represent 407 viruses, including 303 virus species and 104 unclassified?viruses, and 25 viroids, including 20 species and 5 unclassified viroids, as of October 2021, were also introduced. These viruses and viroids are collectively classified into 81 genera within 26 families of 3 kingdoms (Shotokuvirae, Orthornavirae, Pararnavirae) across 2 realms (Monodnaviria and Riboviria). This review also overviewed how Japan’s plant virus/viroid studies have contributed to advance virus/viroid taxonomy. en-copyright= kn-copyright= en-aut-name=FujiShin-ichi en-aut-sei=Fuji en-aut-mei=Shin-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MochizukiTomofumi en-aut-sei=Mochizuki en-aut-mei=Tomofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OkudaMitsuru en-aut-sei=Okuda en-aut-mei=Mitsuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsudaShinya en-aut-sei=Tsuda en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KagiwadaSatoshi en-aut-sei=Kagiwada en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SekineKen-Taro en-aut-sei=Sekine en-aut-mei=Ken-Taro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=UgakiMasashi en-aut-sei=Ugaki en-aut-mei=Masashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NatsuakiKeiko T. en-aut-sei=Natsuaki en-aut-mei=Keiko T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IsogaiMasamichi en-aut-sei=Isogai en-aut-mei=Masamichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MaokaTetsuo en-aut-sei=Maoka en-aut-mei=Tetsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TakeshitaMinoru en-aut-sei=Takeshita en-aut-mei=Minoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=YoshikawaNobuyuki en-aut-sei=Yoshikawa en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MiseKazuyuki en-aut-sei=Mise en-aut-mei=Kazuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=SasayaTakahide en-aut-sei=Sasaya en-aut-mei=Takahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=KubotaKenji en-aut-sei=Kubota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=YamajiYasuyuki en-aut-sei=Yamaji en-aut-mei=Yasuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=IwanamiToru en-aut-sei=Iwanami en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=OhshimaKazusato en-aut-sei=Ohshima en-aut-mei=Kazusato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=KobayashiKappei en-aut-sei=Kobayashi en-aut-mei=Kappei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=HatayaTatsuji en-aut-sei=Hataya en-aut-mei=Tatsuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=SanoTeruo en-aut-sei=Sano en-aut-mei=Teruo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= affil-num=1 en-affil=Faculty of Bioresource Sciences, Akita Prefectural University kn-affil= affil-num=2 en-affil=Graduate School of Life and Environmental Sciences, Osaka Prefecture University kn-affil= affil-num=3 en-affil=Office of the President, National Agriculture and Food Research Organization (NARO) kn-affil= affil-num=4 en-affil=Department of Clinical Plant Science, Faculty of Bioscience and Applied Chemistry kn-affil= affil-num=5 en-affil=Department of Clinical Plant Science, Faculty of Bioscience and Applied Chemistry, Hosei University kn-affil= affil-num=6 en-affil=Faculty of Agriculture, University of the Ryukyus kn-affil= affil-num=7 en-affil=Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo kn-affil= affil-num=8 en-affil=Tokyo University of Agriculture kn-affil= affil-num=9 en-affil=Faculty of Agriculture, Iwate University kn-affil= affil-num=10 en-affil=Institute for Plant Protection, National Agriculture and Food Research Organization (NIPP, NARO) kn-affil= affil-num=11 en-affil=Department of Agricultural and Environmental Sciences, Faculty of Agriculture, University of Miyazak kn-affil= affil-num=12 en-affil=Agri-Innovation Center, Iwate University kn-affil= affil-num=13 en-affil=Graduate School of Agriculture, Kyoto University kn-affil= affil-num=14 en-affil=3 Department of Research Promotion, Institute for Plant Protection, National Agriculture and Food Research Organization (NIPP, NARO) kn-affil= affil-num=15 en-affil=Group of Plant-Microbe Interactions, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=16 en-affil=Division of Core Technology for Pest Control Research, Institute for Plant Protection, National Agriculture and Food Research Organization (NIPP, NARO) kn-affil= affil-num=17 en-affil=Department of Agricultural and Environmental Biology, Graduate School of Agricultural and Life Sciences, The University of Tokyo kn-affil= affil-num=18 en-affil=Faculty of Agriculture, Tokyo University of Agriculture kn-affil= affil-num=19 en-affil=Department of Biological Resource Science, Faculty of Agriculture, Saga University kn-affil= affil-num=20 en-affil=Faculty of Agriculture, Ehime University kn-affil= affil-num=21 en-affil=Research Faculty of Agriculture, Hokkaido University kn-affil= affil-num=22 en-affil=Hirosaki University kn-affil= affil-num=23 en-affil=Group of Plant-Microbe Interactions, Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=95 cd-vols= no-issue=17 article-no= start-page=e00467-21 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=2021810 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Proof of Concept of the Yadokari Nature: a Capsidless Replicase-Encoding but Replication-Dependent Positive-Sense Single-Stranded RNA Virus Hosted by an Unrelated Double-Stranded RNA Virus en-subtitle= kn-subtitle= en-abstract= kn-abstract=Viruses typically encode their own capsids that encase their genomes. However, a capsidless positive-sense single stranded RNA [(+)ssRNA] virus, YkV1, depends on an unrelated double-stranded RNA (dsRNA) virus, YnV1, for encapsidation and replication. en-copyright= kn-copyright= en-aut-name=DasSubha en-aut-sei=Das en-aut-mei=Subha kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AlamMd Mahfuz en-aut-sei=Alam en-aut-mei=Md Mahfuz kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ZhangRui en-aut-sei=Zhang en-aut-mei=Rui kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HisanoSakae en-aut-sei=Hisano en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=5 en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue=1 article-no= start-page=3394 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210209 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Novel urinary glycan profiling by lectin array serves as the biomarkers for predicting renal prognosis in patients with IgA nephropathy en-subtitle= kn-subtitle= en-abstract= kn-abstract=In IgA nephropathy (IgAN), IgA1 molecules are characterized by galactose deficiency in O-glycans. Here, we investigated the association between urinary glycosylation profile measured by 45 lectins at baseline and renal prognosis in 142 patients with IgAN. The primary outcome was estimated glomerular filtration rate (eGFR) decline (>4 mL/min/1.73 m(2)/year), or eGFR >= 30% decline from baseline, or initiation of renal replacement therapies within 3 years. During follow-up (3.4 years, median), 26 patients reached the renal outcome (Group P), while 116 patients were with good renal outcome (Group G). Multivariate logistic regression analyses revealed that lectin binding signals of Erythrina cristagalli lectin (ECA) (odds ratio [OR] 2.84, 95% confidence interval [CI] 1.11-7.28) and Narcissus pseudonarcissus lectin (NPA) (OR 2.32, 95% CI 1.11-4.85) adjusted by age, sex, eGFR, and urinary protein were significantly associated with the outcome, and they recognize Gal(beta 1-4)GlcNAc and high-mannose including Man(alpha 1-6)Man, respectively. The addition of two lectin-binding glycan signals to the interstitial fibrosis/tubular atrophy score further improved the model fitness (Akaike's information criterion) and incremental predictive abilities (c-index, net reclassification improvement, and integrated discrimination improvement). Urinary N-glycan profiling by lectin array is useful in the prediction of IgAN prognosis, since ECA and NPA recognize the intermediate glycans during N-glycosylation of various glycoproteins. en-copyright= kn-copyright= en-aut-name=KawakitaChieko en-aut-sei=Kawakita en-aut-mei=Chieko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiseKoki en-aut-sei=Mise en-aut-mei=Koki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OnishiYasuhiro en-aut-sei=Onishi en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SugiyamaHitoshi en-aut-sei=Sugiyama en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YoshidaMichihiro en-aut-sei=Yoshida en-aut-mei=Michihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=WadaJun en-aut-sei=Wada en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital kn-affil= affil-num=6 en-affil=GlycoTechnica Ltd kn-affil= affil-num=7 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= END start-ver=1.4 cd-journal=joma no-vol=166 cd-vols= no-issue= article-no= start-page=2711 end-page=2722 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=2021727 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A second capsidless hadakavirus strain with 10 positive-sense single-stranded RNA genomic segments from Fusarium nygamai en-subtitle= kn-subtitle= en-abstract= kn-abstract=A unique capsidless virus with a positive-sense, single-stranded RNA genome (hadakavirus 1, HadV1), a member of the extended picorna-like supergroup, was isolated previously from the phytopathogenic fungus Fusarium oxysporum. Here, we describe the molecular and biological characterisation of a second hadakavirus strain from Fusarium nygamai, which has not been investigated in detail previously as a virus host. This virus, hadakavirus 1 strain 1NL (HadV1-1NL), has features similar to the first hadakavirus, HadV1-7n, despite having a different number of segments (10 for HadV1-1NL vs. 11 for HadV1-7n). The 10 genomic RNA segments of HadV1-1NL range in size from 0.9 kb to 2.5 kb. All HadV1-1NL segments show 67% to 86% local nucleotide sequence identity to their HadV1-7n counterparts, whereas HadV1-1NL has no homolog of HadV1-7n RNA8, which encodes a zinc-finger motif. Another interesting feature is the possible coding incapability of HadV1-1NL RNA10. HadV1-1NL was predicted to be capsidless based on the RNase A susceptibility of its replicative form dsRNA. Phenotypic comparison of multiple virus-infected and virus-free single-spore isolates indicated asymptomatic infection by HadV1-1NL. Less-efficient vertical transmission via spores was observed as the infected fungal colonies from which the spores were derived became older, as was observed for HadV1-7n. This study shows a second example of a hadakavirus that appears to have unusual features. en-copyright= kn-copyright= en-aut-name=KhanHaris Ahmed en-aut-sei=Khan en-aut-mei=Haris Ahmed kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SatoYukiyo en-aut-sei=Sato en-aut-mei=Yukiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=JamalAtif en-aut-sei=Jamal en-aut-mei=Atif kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=BhattiMuhammad Faraz en-aut-sei=Bhatti en-aut-mei=Muhammad Faraz kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Crop Diseases Research Institute, National Agricultural Research Centre kn-affil= affil-num=5 en-affil=Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST) kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=27 cd-vols= no-issue=7 article-no= start-page=1126 end-page=1128 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20217 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A patient with human coronavirus NL63 falsely diagnosed with COVID-19; Lesson learned for the importance of definitive diagnosis en-subtitle= kn-subtitle= en-abstract= kn-abstract=The gold standard for the diagnosis of coronavirus disease 2019 (COVID-19) is a nucleic acid detection test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which may occasionally reveal false-positive or false-negative results. Herein, we describe the case of a patient infected with human coronavirus NL63 (HCoV-NL63) who was falsely diagnosed with COVID-19 using the Ampdirect? 2019-nCoV detection kit (Shimadzu Corporation, Japan) and admitted to a COVID-19 hospital ward. We suspected a cross-reaction between HCoV-NL63 and SARS-CoV-2; however, the reported genome sequences of HCoV-NL63 and N1/N2 primers for SARS-CoV-2 do not correspond. Thus, the patient was supposed to be false positive by the instrument, possibly due to contamination. Although the issue of a false-negative result has been the focus of much attention to prevent the spread of the disease, a false positive is fraught with problems as well. Physicians should recognize that unnecessary isolation violates human rights and a careful diagnosis is indispensable when the results of laboratory testing for COVID-19 are unclear, for instance if the duplicate PCR test is partially positive or the CT value is high. en-copyright= kn-copyright= en-aut-name=OtsukaYuki en-aut-sei=Otsuka en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HagiyaHideharu en-aut-sei=Hagiya en-aut-mei=Hideharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NakanoYasuhiro en-aut-sei=Nakano en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OmuraDaisuke en-aut-sei=Omura en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HasegawaKou en-aut-sei=Hasegawa en-aut-mei=Kou kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamadaHaruto en-aut-sei=Yamada en-aut-mei=Haruto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IioKoji en-aut-sei=Iio en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HondaTomoyuki en-aut-sei=Honda en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OtsukaFumio en-aut-sei=Otsuka en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Laboratory Medicine, Okayama City Hospital kn-affil= affil-num=7 en-affil=Microbiology Division, Clinical Laboratory, Okayama University Hospital kn-affil= affil-num=8 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Human coronavirus kn-keyword=Human coronavirus en-keyword=Coronavirus disease 2019 kn-keyword=Coronavirus disease 2019 en-keyword=Severe acute respiratory syndrome coronavirus 2 kn-keyword=Severe acute respiratory syndrome coronavirus 2 END start-ver=1.4 cd-journal=joma no-vol=8 cd-vols= no-issue= article-no= start-page=668059 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210524 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Novel Urinary Glycan Biomarkers Predict Cardiovascular Events in Patients With Type 2 Diabetes: A Multicenter Prospective Study With 5-Year Follow Up (U-CARE Study 2) en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background: Although various biomarkers predict cardiovascular event (CVE) in patients with diabetes, the relationship of urinary glycan profile with CVE in patients with diabetes remains unclear. Methods: Among 680 patients with type 2 diabetes, we examined the baseline urinary glycan signals binding to 45 lectins with different specificities. Primary outcome was defined as CVE including cardiovascular disease, stroke, and peripheral arterial disease. Results: During approximately a 5-year follow-up period, 62 patients reached the endpoint. Cox proportional hazards analysis revealed that urinary glycan signals binding to two lectins were significantly associated with the outcome after adjustment for known indicators of CVE and for false discovery rate, as well as increased model fitness. Hazard ratios for these lectins (+1 SD for the glycan index) were UDA (recognizing glycan: mixture of Man5 to Man9): 1.78 (95% CI: 1.24-2.55, P = 0.002) and Calsepa [High-Man (Man2-6)]: 1.56 (1.19-2.04, P = 0.001). Common glycan binding to these lectins was high-mannose type of N-glycans. Moreover, adding glycan index for UDA to a model including known confounders improved the outcome prediction [Difference of Harrel's C-index: 0.028 (95% CI: 0.001-0.055, P = 0.044), net reclassification improvement at 5-year risk increased by 0.368 (0.045-0.692, P = 0.026), and the Akaike information criterion and Bayesian information criterion decreased from 725.7 to 716.5, and 761.8 to 757.2, respectively]. Conclusion: The urinary excretion of high-mannose glycan may be a valuable biomarker for improving prediction of CVE in patients with type 2 diabetes, and provides the rationale to explore the mechanism underlying abnormal N-glycosylation occurring in patients with diabetes at higher risk of CVE. en-copyright= kn-copyright= en-aut-name=MiseKoki en-aut-sei=Mise en-aut-mei=Koki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ImamuraMariko en-aut-sei=Imamura en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamaguchiSatoshi en-aut-sei=Yamaguchi en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WatanabeMayu en-aut-sei=Watanabe en-aut-mei=Mayu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HiguchiChigusa en-aut-sei=Higuchi en-aut-mei=Chigusa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KatayamaAkihiro en-aut-sei=Katayama en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MiyamotoSatoshi en-aut-sei=Miyamoto en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UchidaHaruhito A. en-aut-sei=Uchida en-aut-mei=Haruhito A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NakatsukaAtsuko en-aut-sei=Nakatsuka en-aut-mei=Atsuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=EguchiJun en-aut-sei=Eguchi en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=HidaKazuyuki en-aut-sei=Hida en-aut-mei=Kazuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=NakatoTatsuaki en-aut-sei=Nakato en-aut-mei=Tatsuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=ToneAtsuhito en-aut-sei=Tone en-aut-mei=Atsuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=TeshigawaraSanae en-aut-sei=Teshigawara en-aut-mei=Sanae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=MatsuokaTakashi en-aut-sei=Matsuoka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=KameiShinji en-aut-sei=Kamei en-aut-mei=Shinji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=MurakamiKazutoshi en-aut-sei=Murakami en-aut-mei=Kazutoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=ShimizuIkki en-aut-sei=Shimizu en-aut-mei=Ikki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=MiyashitaKatsuhiro en-aut-sei=Miyashita en-aut-mei=Katsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=AndoShinichiro en-aut-sei=Ando en-aut-mei=Shinichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=NunoueTomokazu en-aut-sei=Nunoue en-aut-mei=Tomokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= en-aut-name=YoshidaMichihiro en-aut-sei=Yoshida en-aut-mei=Michihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=22 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=23 ORCID= en-aut-name=ShikataKenichi en-aut-sei=Shikata en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=24 ORCID= en-aut-name=WadaJun en-aut-sei=Wada en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=25 ORCID= affil-num=1 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Diabetes Center, Okayama University Hospital kn-affil= affil-num=7 en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital kn-affil= affil-num=8 en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Diabetology and Metabolism, National Hospital Organization Okayama Medical Center kn-affil= affil-num=12 en-affil=Okayama Saiseikai General Hospital kn-affil= affil-num=13 en-affil=Okayama Saiseikai General Hospital kn-affil= affil-num=14 en-affil=Okayama Saiseikai General Hospital kn-affil= affil-num=15 en-affil=Kurashiki Central Hospital kn-affil= affil-num=16 en-affil=Kurashiki Central Hospital kn-affil= affil-num=17 en-affil=Kurashiki Central Hospital kn-affil= affil-num=18 en-affil=The Sakakibara Heart Institute of Okayama kn-affil= affil-num=19 en-affil=Japanese Red Cross Okayama Hospital kn-affil= affil-num=20 en-affil=Okayama City General Medical Center kn-affil= affil-num=21 en-affil=Nunoue Clinic kn-affil= affil-num=22 en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital kn-affil= affil-num=23 en-affil=GlycoTechnica Ltd. kn-affil= affil-num=24 en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital kn-affil= affil-num=25 en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=cardiovascular event kn-keyword=cardiovascular event en-keyword=diabetes kn-keyword=diabetes en-keyword=lectins kn-keyword=lectins en-keyword=N-glycans kn-keyword=N-glycans en-keyword=urinary biomarkers kn-keyword=urinary biomarkers END start-ver=1.4 cd-journal=joma no-vol=132 cd-vols= no-issue=3 article-no= start-page=131 end-page=143 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hepatitis C virus (HCV) : Development of anti-HCV agents and anti-HCV therapy kn-title=Ｃ型肝炎ウイルス（HCV）：抗 HCV 剤の開発と抗 HCV 療法 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name=加藤宣之 kn-aut-sei=加藤 kn-aut-mei=宣之 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 en-keyword=インターフェロン kn-keyword=インターフェロン en-keyword=リバビリン kn-keyword=リバビリン en-keyword=HCVレプリコンシステム kn-keyword=HCVレプリコンシステム en-keyword=抗HCVアッセイシステム kn-keyword=抗HCVアッセイシステム en-keyword= DAA kn-keyword= DAA END start-ver=1.4 cd-journal=joma no-vol=75 cd-vols= no-issue=2 article-no= start-page=213 end-page=218 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=202104 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A Case of Dual-pathology Hepatocellular Carcinoma (HCC) and Cholangiolocellular Carcinoma (CoCC) after Eradication of Hepatitis C Virus (HCV) Infection en-subtitle= kn-subtitle= en-abstract= kn-abstract=A 75-year-old Japanese man visited our hospital for further examination of liver tumors. He had a history of successful hepatitis C virus (HCV) eradication and therapy for hepatocellular carcinoma (HCC) at another hospital. Magnetic resonance imaging (MRI) revealed two tumors in the liver. He underwent anterior inferior (S5) and posterior inferior (S6) subsegmentectomy of the liver. Microscopic examination found that one tumor was HCC while the other was cholangiolocellular carcinoma (CoCC). We experienced a rare case of liver cancer with two synchronous pathologies, HCC and CoCC. en-copyright= kn-copyright= en-aut-name=MiyashitaManabi en-aut-sei=Miyashita en-aut-mei=Manabi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SaragaiYousuke en-aut-sei=Saragai en-aut-mei=Yousuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FujimotoTsuyoshi en-aut-sei=Fujimoto en-aut-mei=Tsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TanakaShouichi en-aut-sei=Tanaka en-aut-mei=Shouichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=AokiHideki en-aut-sei=Aoki en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SatoYumiko en-aut-sei=Sato en-aut-mei=Yumiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Department of Hepatology, National Hospital Organaization of Iwakuni Clinical Center kn-affil= affil-num=2 en-affil=Department of Gastroenterology, National Hospital Organaization of Iwakuni Clinical Center kn-affil= affil-num=3 en-affil=Department of Gastroenterology, National Hospital Organaization of Iwakuni Clinical Center kn-affil= affil-num=4 en-affil=Department of Gastroenterology, National Hospital Organaization of Iwakuni Clinical Center kn-affil= affil-num=5 en-affil=Department of Surgery, National Hospital Organaization of Iwakuni Clinical Center kn-affil= affil-num=6 en-affil=Department of Pathology, National Hospital Organaization of Iwakuni Clinical Center kn-affil= END start-ver=1.4 cd-journal=joma no-vol=10 cd-vols= no-issue=2 article-no= start-page=100 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210131 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Identification of an RNA Silencing Suppressor Encoded by a Symptomless Fungal Hypovirus, Cryphonectria Hypovirus 4 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Previously, we have reported the ability of a symptomless hypovirus Cryphonectria hypovirus 4 (CHV4) of the chestnut blight fungus to facilitate stable infection by a co-infecting mycoreovirus 2 (MyRV2)?likely through the inhibitory effect of CHV4 on RNA silencing (Aulia et al., Virology, 2019). In this study, the N-terminal portion of the CHV4 polyprotein, termed p24, is identified as an autocatalytic protease capable of suppressing host antiviral RNA silencing. Using a bacterial expression system, CHV4 p24 is shown to cleave autocatalytically at the di-glycine peptide (Gly214-Gly215) of the polyprotein through its protease activity. Transgenic expression of CHV4 p24 in Cryphonectria parasitica suppresses the induction of one of the key genes of the antiviral RNA silencing, dicer-like 2, and stabilizes the infection of RNA silencing-susceptible virus MyRV2. This study shows functional similarity between CHV4 p24 and its homolog p29, encoded by the symptomatic prototype hypovirus CHV1. en-copyright= kn-copyright= en-aut-name=AuliaAnnisa en-aut-sei=Aulia en-aut-mei=Annisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HyodoKiwamu en-aut-sei=Hyodo en-aut-mei=Kiwamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HisanoSakae en-aut-sei=Hisano en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HillmanBradley I. en-aut-sei=Hillman en-aut-mei=Bradley I. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=5 en-affil=Plant Biology and Pathology, Rutgers University kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= en-keyword=mycovirus kn-keyword=mycovirus en-keyword=reovirus kn-keyword=reovirus en-keyword=hypovirus kn-keyword=hypovirus en-keyword=Cryphonectria parasitica kn-keyword=Cryphonectria parasitica en-keyword=co-infection kn-keyword=co-infection en-keyword=RNA silencing kn-keyword=RNA silencing en-keyword=RNAi suppressor kn-keyword=RNAi suppressor en-keyword=chestnut blight fungus kn-keyword=chestnut blight fungus en-keyword=Dicer kn-keyword=Dicer END start-ver=1.4 cd-journal=joma no-vol=554 cd-vols= no-issue= article-no= start-page=55 end-page=62 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=202102 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Cryphonectria nitschkei chrysovirus 1 with unique molecular features and a very narrow host range en-subtitle= kn-subtitle= en-abstract= kn-abstract=Cryphonectria nitschkei chrysovirus 1 (CnCV1), was described earlier from an ascomycetous fungus, Cryphonectria nitschkei strain OB5/11, collected in Japan; its partial sequence was reported a decade ago. Complete sequencing of the four genomic dsRNA segments revealed molecular features similar to but distinct from previously reported members of the family Chrysoviridae. Unique features include the presence of a mini-cistron preceding the major large open reading frame in each genomic segment. Common features include the presence of CAA repeats in the 5′-untranslated regions and conserved terminal sequences. CnCV1-OB5/11 could be laterally transferred to C. nitschkei and its relatives C. radicalis and C. naterciae via coculturing, virion transfection and protoplast fusion, but not to fungal species other than the three species mentioned above, even within the genus Cryphonectria, suggesting a very narrow host range. Phenotypic comparison of a few sets of CnCV1-infected and -free isogenic strains showed symptomless infection in new hosts. en-copyright= kn-copyright= en-aut-name=ShahiSabitree en-aut-sei=Shahi en-aut-mei=Sabitree kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ChibaSotaro en-aut-sei=Chiba en-aut-mei=Sotaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=Graduate School of Bioagricultural Sciences, Nagoya University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= en-keyword=Cryphonectria nitschkei kn-keyword=Cryphonectria nitschkei en-keyword=Cryphonectria parasitica kn-keyword=Cryphonectria parasitica en-keyword=Cryphonectria radicalis kn-keyword=Cryphonectria radicalis en-keyword=Chrysovirus kn-keyword=Chrysovirus en-keyword=Fungal virus kn-keyword=Fungal virus en-keyword=dsRNA kn-keyword=dsRNA en-keyword=Host range kn-keyword=Host range END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue=1 article-no= start-page=5627 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201106 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Establishment of Neurospora crassa as a model organism for fungal virology en-subtitle= kn-subtitle= en-abstract= kn-abstract=The filamentous fungus Neurospora crassa is used as a model organism for genetics, developmental biology and molecular biology. Remarkably, it is not known to host or to be susceptible to infection with any viruses. Here, we identify diverse RNA viruses in N. crassa and other Neurospora species, and show that N. crassa supports the replication of these viruses as well as some viruses from other fungi. Several encapsidated double-stranded RNA viruses and capsid-less positive-sense single-stranded RNA viruses can be experimentally introduced into N. crassa protoplasts or spheroplasts. This allowed us to examine viral replication and RNAi-mediated antiviral responses in this organism. We show that viral infection upregulates the transcription of RNAi components, and that Dicer proteins (DCL-1, DCL-2) and an Argonaute (QDE-2) participate in suppression of viral replication. Our study thus establishes N. crassa as a model system for the study of host-virus interactions. The fungus Neurospora crassa is a model organism for the study of various biological processes, but it is not known to be infected by any viruses. Here, Honda et al. identify RNA viruses that infect N. crassa and examine viral replication and RNAi-mediated antiviral responses, thus establishing this fungus as a model for the study of host-virus interactions. en-copyright= kn-copyright= en-aut-name=HondaShinji en-aut-sei=Honda en-aut-mei=Shinji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=Eusebio-CopeAna en-aut-sei=Eusebio-Cope en-aut-mei=Ana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MiyashitaShuhei en-aut-sei=Miyashita en-aut-mei=Shuhei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YokoyamaAyumi en-aut-sei=Yokoyama en-aut-mei=Ayumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=AuliaAnnisa en-aut-sei=Aulia en-aut-mei=Annisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ShahiSabitree en-aut-sei=Shahi en-aut-mei=Sabitree kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil=Faculty of Medical Sciences, University of Fukui kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=3 en-affil=Graduate School of Agricultural Science, Tohoku University kn-affil= affil-num=4 en-affil=Faculty of Medical Sciences, University of Fukui kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=7 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=8 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= en-keyword=Fungal biology kn-keyword=Fungal biology en-keyword=Virus?host interactions kn-keyword=Virus?host interactions END start-ver=1.4 cd-journal=joma no-vol=132 cd-vols= no-issue=2 article-no= start-page=60 end-page=67 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200803 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hepatitis C virus (HCV)：Diversity and variation of RNA genome kn-title=C型肝炎ウイルス（HCV）：RNAゲノムの多様性と変異性 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name=加藤宣之 kn-aut-sei=加藤 kn-aut-mei=宣之 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 en-keyword=HCV ゲノム kn-keyword=HCV ゲノム en-keyword=レプリコン複製細胞 kn-keyword=レプリコン複製細胞 en-keyword=長期継代培養 kn-keyword=長期継代培養 en-keyword=遺伝子解析 kn-keyword=遺伝子解析 en-keyword=準種 kn-keyword=準種 END start-ver=1.4 cd-journal=joma no-vol=154 cd-vols= no-issue=1 article-no= start-page=37 end-page=45 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20081206 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Identification and characterization of structural proteins of orchid fleck virus en-subtitle= kn-subtitle= en-abstract= kn-abstract=Orchid fleck virus (OFV) has a bipartite negative-sense RNA genome with sequence similarities to plant rhabdoviruses. The non-enveloped bullet-shaped particles of OFV are similar to those of the internal ribonucleoprotein (RNP)-M protein structure of rhabdoviruses, but they are about half the size of typical plant rhabdoviruses. Purified preparations contained intact bullet-shaped and filamentous particles. The filamentous particles showed a tightly coiled coil structure or a coiled structure with a helical twist, which resembles the RNP complex of rhabdoviruses. OFV bullet-shaped particles were structurally stable in solutions containing 2% Triton X-100 and 0.8 M NaCl. Western blot analyses revealed that the bullet-shaped particles contained N, P and M proteins, while filamentous particles contained mainly N and P proteins. In addition, a small amount of the L protein was detected in both types of particles. Thus, the structural proteins of OFV have properties similar to those of rhabdoviruses, except that the particles are non-enveloped and are relatively resistant to detergent-treatment under high-salt conditions. en-copyright= kn-copyright= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaedaTakanori en-aut-sei=Maeda en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TamadaTetsuo en-aut-sei=Tamada en-aut-mei=Tetsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil=Research Institute for Bioresources, Okayama University kn-affil= affil-num=2 en-affil=College of Bioresource Sciences, Nihon University kn-affil= affil-num=3 en-affil=Research Institute for Bioresources, Okayama University kn-affil= en-keyword=Rabies kn-keyword=Rabies en-keyword=ORF4 Protein kn-keyword=ORF4 Protein en-keyword=Sucrose Density Gradient Centrifugation kn-keyword=Sucrose Density Gradient Centrifugation en-keyword=Coil Coil Structure kn-keyword=Coil Coil Structure en-keyword=Potential Glycosylation Site kn-keyword=Potential Glycosylation Site END start-ver=1.4 cd-journal=joma no-vol=1 cd-vols= no-issue= article-no= start-page=100001 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200720 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Dicer monitoring in a model filamentous fungus host, Cryphonectria parasitica en-subtitle= kn-subtitle= en-abstract= kn-abstract=The ascomycete Cryphonectria parasitica has served as a model filamentous fungus for studying virus host interactions because of its susceptibility to diverse viruses, its genetic manipulability and the availability of many biological and molecular tools. Cryphonectria prasitica is known to activate antiviral RNA silencing upon infection by some viruses via transcriptional up-regulation of key RNA silencing genes. Here, utilizing a newly developed GFP-based reporter system to monitor dicer-like 2 (dcl2) transcript levels, we show different levels of antiviral RNA silencing activation by different viruses. Some viruses such as mycoreovirus 1, a suppressor-lacking mutant of Cryphonectria hypovirus 1 (CHV1-Δp69) and Rosellinia necatrix partitivirus 11 (RnPV11) highly induced RNA silencing, while others such as CHV3, Rosellinia necatrix victorivirus 1 and RnPV19 did not. There was considerable variation in dcl2 induction by different members within the family Hypoviridae with positive-sense single-stranded RNA genomes or Partitiviridae with double-stranded RNA genomes. Northern blotting and an in vitro Dicer assay developed recently by us using mycelial homogenates validated the reporter assay results for several representative virus strains. Taken together, this study represents a development in the monitoring of Dicer activity in virus-infected C. parasitica. en-copyright= kn-copyright= en-aut-name=AuliaAnnisa en-aut-sei=Aulia en-aut-mei=Annisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TabaraMidori en-aut-sei=Tabara en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TelengechPaul en-aut-sei=Telengech en-aut-mei=Paul kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FukuharaToshiyuki en-aut-sei=Fukuhara en-aut-mei=Toshiyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil=Tokyo University of Agriculture and Technology, Department of Applied Biological Sciences kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=4 en-affil=Tokyo University of Agriculture and Technology, Department of Applied Biological Sciences kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= en-keyword=Dicer kn-keyword=Dicer en-keyword=RNA silencing kn-keyword=RNA silencing en-keyword=Fungal virus kn-keyword=Fungal virus en-keyword=RNA virus kn-keyword=RNA virus en-keyword=Antiviral defense kn-keyword=Antiviral defense END start-ver=1.4 cd-journal=joma no-vol=132 cd-vols= no-issue=1 article-no= start-page=13 end-page=17 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Natural history and pathogenicity of herpesviruses kn-title=ヘルペスウイルスの自然史と病態 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name=山田雅夫 kn-aut-sei=山田 kn-aut-mei=雅夫 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　病原ウイルス学 en-keyword= ヘルペスウイルス kn-keyword= ヘルペスウイルス en-keyword= 自然史 kn-keyword= 自然史 en-keyword=病態 kn-keyword=病態 en-keyword=潜伏感染 kn-keyword=潜伏感染 en-keyword=再活性化 kn-keyword=再活性化 END start-ver=1.4 cd-journal=joma no-vol=92 cd-vols= no-issue=12 article-no= start-page=3689 end-page=3696 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200407 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The aim of the measurement of Epstein‐Barr virus DNA in hydroa vacciniforme and hypersensitivity to mosquito bites en-subtitle= kn-subtitle= en-abstract= kn-abstract=Epstein‐Barr virus (EBV) DNA load in the blood increases in posttransplant lymphoproliferative disorders and chronic active EBV infection. In this report, we analyzed the EBV DNA load in the peripheral blood mononuclear cells (PBMCs) and plasma of patients with hydroa vacciniforme (HV) and/or hypersensitivity to mosquito bites (HMB) to understand the clinical significance of EBV DNA load. All 30 patients showed high DNA loads in the PBMCs over the cut‐off level. Of 16 plasma samples, extremely high in two samples obtained from patients with hemophagocytic lymphohistiocytosis (HLH). The amount of cell‐free DNA in plasma was correlated to the serum levels of lactate dehydrogenase and inversely correlated to platelet counts. These results indicate that the EBV DNA load in PBMCs can provide one of the diagnostic indicators for HV and HMB and marked elevation of cell‐free EBV DNA in plasma might be related to cytolysis such as that observed in HLH. en-copyright= kn-copyright= en-aut-name=MiyakeTomoko en-aut-sei=Miyake en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IwatsukiKeiji en-aut-sei=Iwatsuki en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HiraiYoji en-aut-sei=Hirai en-aut-mei=Yoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamamotoTakenobu en-aut-sei=Yamamoto en-aut-mei=Takenobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HamadaToshihisa en-aut-sei=Hamada en-aut-mei=Toshihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Fujii Kazuyasu en-aut-sei=Fujii en-aut-mei= Kazuyasu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=mamuraHideaki en-aut-sei=mamura en-aut-mei=Hideaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MorizaneShin en-aut-sei=Morizane en-aut-mei=Shin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=5 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Department of Pediatrics, Faculty of Medicine, University of Miyazaki kn-affil= affil-num=8 en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=Epstein-Barr Virus DNA load kn-keyword=Epstein-Barr Virus DNA load en-keyword=hydroa vaccniforme kn-keyword=hydroa vaccniforme en-keyword=hypersensitivity to mosquito bite kn-keyword=hypersensitivity to mosquito bite en-keyword=hemophagocytic lymphohistiocytosis kn-keyword=hemophagocytic lymphohistiocytosis END start-ver=1.4 cd-journal=joma no-vol=81 cd-vols= no-issue=8 article-no= start-page=1191 end-page=1196 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190824 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Risk assessment for hepatitis E virus infection from domestic pigs introduced into an experimental animal facility in a medical school en-subtitle= kn-subtitle= en-abstract= kn-abstract= Hepatitis E virus (HEV) is known to cause zoonotic infections from pigs, wild boars and deer. Domestic pigs have been used as an experimental animal model in medical research and training; however, the risks of HEV infection from pigs during animal experiments are largely unknown. Here, we retrospectively investigated the seroprevalence and detection rates of viral RNA in 73 domestic pigs (average 34.5 kg) introduced into an animal experimental facility in a medical school during 2012-2016. We detected anti-HEV immunoglobulin G antibodies in 24 of 73 plasma samples (32.9%), though none of the samples were positive for viral RNA. Plasma samples of 18 pigs were sequentially monitored and were classified into four patterns: sustained positive (5 pigs), sustained negative (5 pigs), conversion to positive (6 pigs) and conversion to negative (2 pigs). HEV genomes were detected in 2 of 4 liver samples from pigs that were transported from the same farm during 2016-2017. Two viral sequences of the overlapping open reading frame (ORF) 2/3 region (97 bp) were identical and phylogenetically fell into genotype 3. A 459-bp length of the ORF2 region of an amplified fragment from a pig transported in 2017 was clustered with the wbJYG1 isolate (subgenotype 3b) with 91.5% (420/459 bp) nucleotide identity. Based on our results, we suggest that domestic pigs introduced into animal facilities carry a potential risk of HEV infection to researchers, trainees and facility staff. Continuous surveillance and precautions are important to prevent HEV infection in animal facilities. en-copyright= kn-copyright= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HirayamaHaruko en-aut-sei=Hirayama en-aut-mei=Haruko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanakaSatsuki en-aut-sei=Tanaka en-aut-mei=Satsuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YataNorio en-aut-sei=Yata en-aut-mei=Norio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NambaHikaru en-aut-sei=Namba en-aut-mei=Hikaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=YonemitsuKenzo en-aut-sei=Yonemitsu en-aut-mei=Kenzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MaedaKen en-aut-sei=Maeda en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MominokiKatsumi en-aut-sei=Mominoki en-aut-mei=Katsumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Animal Resources, Advanced Science Research Center, Okayama University kn-affil= affil-num=3 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Animal Resources, Advanced Science Research Center, Okayama University kn-affil= affil-num=5 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University kn-affil= affil-num=8 en-affil=Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University kn-affil= affil-num=9 en-affil=Department of Animal Resources, Advanced Science Research Center, Okayama University kn-affil= affil-num=10 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, kn-affil= en-keyword=animal experimental facility kn-keyword=animal experimental facility en-keyword=domestic pig kn-keyword=domestic pig en-keyword=hepatitis E virus kn-keyword=hepatitis E virus en-keyword=zoonosis kn-keyword=zoonosis END start-ver=1.4 cd-journal=joma no-vol=100 cd-vols= no-issue=9 article-no= start-page=1269 end-page=1270 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190901 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ICTV Virus Taxonomy Profile: Megabirnaviridae en-subtitle= kn-subtitle= en-abstract= kn-abstract= Megabirnaviridae is a family of non-enveloped spherical viruses with dsRNA genomes of two linear segments, each of 7.2-8.9 kbp, comprising 16.1 kbp in total. The genus Megabirnavirus includes the species Rosellinia necatrix megabirnavirus 1, the exemplar isolate of which infects the white root rot fungus (Rosellinia necatrix) to which it confers hypovirulence. Megabirnaviruses are characterized by their bisegmented genome with large 5'-untranslated regions (1.6?kb) upstream of both 5'-proximal coding strand ORFs, and large protrusions on the particle surface. This is a summary of the ICTV Report on the family Megabirnaviridae, which is available at ictv.global/report/megabirnaviridae. en-copyright= kn-copyright= en-aut-name=SatoYukiyo en-aut-sei=Sato en-aut-mei=Yukiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyazakiNaoyuki en-aut-sei=Miyazaki en-aut-mei=Naoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KanematsuSatoko en-aut-sei=Kanematsu en-aut-mei=Satoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=XieJiatao en-aut-sei=Xie en-aut-mei=Jiatao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=GhabrialSaid A. en-aut-sei=Ghabrial en-aut-mei=Said A. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HillmanBradley I. en-aut-sei=Hillman en-aut-mei=Bradley I. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources, Okayama University kn-affil= affil-num=2 en-affil= Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance, University of Tsukuba kn-affil= affil-num=3 en-affil= National Agriculture and Food Research Organization (NARO) Headquarters kn-affil= affil-num=4 en-affil=College of Plant Science and Technology, Huazhong Agricultural University kn-affil= affil-num=5 en-affil=Department of Plant Pathology, University of Kentucky kn-affil= affil-num=6 en-affil=Department of Plant Biology and Pathology, Rutgers University kn-affil= affil-num=7 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= en-keyword=ICTV Report kn-keyword=ICTV Report en-keyword=Megabirnaviridae kn-keyword=Megabirnaviridae en-keyword=taxonomy kn-keyword=taxonomy END start-ver=1.4 cd-journal=joma no-vol=159 cd-vols= no-issue=1 article-no= start-page=163 end-page=166 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130716 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Complete genome sequence of Habenaria mosaic virus, a new potyvirus infecting a terrestrial orchid (Habenaria radiata) in Japan en-subtitle= kn-subtitle= en-abstract= kn-abstract= The complete genomic sequence of Habenaria mosaic virus (HaMV), which infects terrestrial orchids (Habenaria radiata), has been determined. The genome is composed of 9,499 nucleotides excluding the 3'-terminal poly(A) tail, encoding a large polyprotein of 3,054 amino acids with the genomic features typical of a potyvirus. Putative proteolytic cleavage sites were identified by sequence comparison to those of known potyviruses. The HaMV polyprotein showed 58 % amino acid sequence identity to that encoded by the most closely related potyvirus, tobacco vein banding mosaic virus. Phylogenetic analysis of the polyprotein amino acid sequence and its coding sequences confirmed that HaMV formed a cluster with the chilli veinal mottle virus group, most of which infect solanaceous plants. These results suggest that HaMV is a distinct member of the genus Potyvirus. en-copyright= kn-copyright= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaedaTakanori en-aut-sei=Maeda en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=I Wayan Gara en-aut-sei=I Wayan Gara en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ChibaSotaro en-aut-sei=Chiba en-aut-mei=Sotaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MaruyamaKazuyuki en-aut-sei=Maruyama en-aut-mei=Kazuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TamadaTetsuo en-aut-sei=Tamada en-aut-mei=Tetsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=2 en-affil=College of Bioresource SciencesNihon University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=7 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=160 cd-vols= no-issue=8 article-no= start-page=2099 end-page=104 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=20150531 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Cymbidium chlorotic mosaic virus, a new sobemovirus isolated from a spring orchid (Cymbidium goeringii) in Japan. en-subtitle= kn-subtitle= en-abstract= kn-abstract=Cymbidium chlorotic mosaic virus (CyCMV), isolated from a spring orchid (Cymbidium goeringii), was characterized molecularly. CyCMV isometric virions comprise a single, positive-strand RNA genome of 4,083 nucleotides and 30-kDa coat protein. The virus genome contains five overlapping open reading frames with a genomic organization similar to that of sobemoviruses. BLAST searches and phylogenetic analysis revealed that CyCMV is most closely related to papaya lethal yellowing virus, a proposed dicot-infecting sobemovirus (58.8 % nucleotide sequence identity), but has a relatively distant relationship to monocot-infecting sobemoviruses, with only modest sequence identities. This suggests that CyCMV is a new monocot-infecting member of the floating genus Sobemovirus. en-copyright= kn-copyright= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakemotoShogo en-aut-sei=Takemoto en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MaruyamaKazuyuki en-aut-sei=Maruyama en-aut-mei=Kazuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ChibaSotaro en-aut-sei=Chiba en-aut-mei=Sotaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=Ida Bagus Andika en-aut-sei=Ida Bagus Andika en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SuzukiNobuhiro en-aut-sei=Suzuki en-aut-mei=Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources (IPSR)Okayama University kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=177 cd-vols= no-issue=1 article-no= start-page=75 end-page=86 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201310 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Characterization of burdock mottle virus, a novel member of the genus Benyvirus, and the identification of benyvirus-related sequences in the plant and insect genomes. en-subtitle= kn-subtitle= en-abstract= kn-abstract= The complete nucleotide sequence of the burdock mottle virus (BdMoV) isolated from an edible burdock plant (Arctium lappa) in Japan has been determined. BdMoV has a bipartite genome, whose organization is similar to RNA1 and RNA2 of benyviruses, beet necrotic yellow vein virus (BNYVV), beet soil-borne mosaic virus (BSBMV), and rice stripe necrosis virus (RSNV). BdMoV RNA1 (7038 nt) contains a single open reading frame (ORF) encoding a 249-kDa polypeptide that consists of methyl-transferase, helicase, papain-like protease, AlkB-like, and RNA-dependent RNA polymerase domains. The AlkB-like domain sequence is not present in the proteins encoded by other known benyviruses, but is found in replication-associated proteins of viruses mainly belonging to the families Alfaflexiviridae and Betaflexiviridae. BdMoV RNA2 (4315 nt) contains six ORFs that are similar to those of benyviruses: these are coat protein (CP), CP readthrough, triple gene block movement and cysteine-rich proteins. Phylogenetic analyses showed that BdMoV is more closely related to BNYVV and BSBMV than to RSNV. Database searches showed that benyvirus replicase-related sequences are present in the chromosomes of a chickpea plant (Cicer arietinum) and a blood-sucking insect (Rhodnius prolixus). Some other benyvirus-related sequences are found in the transcriptome shotgun libraries of a few species of plants and a bark beetle. Our results show that BdMoV is a distinct species of the genus Benyvirus and that ancestral and extant benyviruses may have infected or currently infect a wide range of hosts, including plants and insects. en-copyright= kn-copyright= en-aut-name=KondoHideki en-aut-sei=Kondo en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HiranoShuichi en-aut-sei=Hirano en-aut-mei=Shuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ChibaSotaro en-aut-sei=Chiba en-aut-mei=Sotaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=AndikaIda Bagus en-aut-sei=Andika en-aut-mei=Ida Bagus kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HiraiMakoto en-aut-sei=Hirai en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MaedaTakanori en-aut-sei=Maeda en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TamadaTetsuo en-aut-sei=Tamada en-aut-mei=Tetsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=3 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=4 en-affil=Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences kn-affil= affil-num=5 en-affil=Department of Parasitology, Graduate School of Medicine, Gunma University kn-affil= affil-num=6 en-affil=Formerly College of Bioresource Sciences, Nihon University kn-affil= affil-num=7 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= en-keyword=AlkB kn-keyword=AlkB en-keyword=Benyvirus kn-keyword=Benyvirus en-keyword=Burdock mottle virus kn-keyword=Burdock mottle virus en-keyword=Endogenous viral element kn-keyword=Endogenous viral element en-keyword=Paleovirology kn-keyword=Paleovirology en-keyword=Transcriptome shotgun assembly kn-keyword=Transcriptome shotgun assembly END start-ver=1.4 cd-journal=joma no-vol=533 cd-vols= no-issue= article-no= start-page=125 end-page=136 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190731 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Two novel fungal negative-strand RNA viruses related to mymonaviruses and phenuiviruses in the shiitake mushroom (Lentinula edodes) en-subtitle= kn-subtitle= en-abstract= kn-abstract=Abstract There is still limited information on the diversity of (?)ssRNA viruses that infect fungi. Here, we have discovered two novel (?)ssRNA mycoviruses in the shiitake mushroom (Lentinula edodes). The first virus has a monopartite RNA genome and relates to that of mymonaviruses (Mononegavirales), especially to Hubei rhabdo-like virus 4 from arthropods and thus designated as Lentinula edodes negative-strand RNA virus 1. The second virus has a putative bipartite RNA genome and is related to the recently discovered bipartite or tripartite phenui-like viruses (Bunyavirales) associated with plants and ticks, and designated as Lentinula edodes negative-strand RNA virus 2 (LeNSRV2). LeNSRV2 is likely the first segmented (?)ssRNA virus known to infect fungi. Its smaller RNA segment encodes a putative nucleocapsid and a plant MP-like protein using a potential ambisense coding strategy. These findings enhance our understanding of the diversity, evolution and spread of (?)ssRNA viruses in fungi. en-copyright= kn-copyright= en-aut-name=Lin Yu-Hsin en-aut-sei=Lin en-aut-mei= Yu-Hsin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=Fujita Miki en-aut-sei=Fujita en-aut-mei= Miki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=Chiba Sotaro en-aut-sei=Chiba en-aut-mei= Sotaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Hyodo Kiwamu en-aut-sei=Hyodo en-aut-mei= Kiwamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=Andika Ida Bagus en-aut-sei=Andika en-aut-mei= Ida Bagus kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Suzuki Nobuhiro en-aut-sei=Suzuki en-aut-mei= Nobuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=Kondo Hideki en-aut-sei=Kondo en-aut-mei= Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=2 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=3 en-affil=Graduate School of Bioagricultural Sciences, Nagoya University kn-affil= affil-num=4 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=5 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=6 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= affil-num=7 en-affil=Institute of Plant Science and Resources (IPSR), Okayama University kn-affil= en-keyword=Ambisense kn-keyword=Ambisense en-keyword=Bipartite genome kn-keyword=Bipartite genome en-keyword=Endogenous virus element kn-keyword=Endogenous virus element en-keyword=Evolution kn-keyword=Evolution en-keyword=High-throughput sequencing kn-keyword=High-throughput sequencing en-keyword=Lentinula edodes kn-keyword=Lentinula edodes en-keyword=Mymonaviridae kn-keyword=Mymonaviridae en-keyword=Negative-strand RNA virus kn-keyword=Negative-strand RNA virus en-keyword=Phenuiviridae kn-keyword=Phenuiviridae en-keyword=Shitake mushroom kn-keyword=Shitake mushroom END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=インフルエンザ肺炎モデルマウスに対する抗HMGB1抗体とペラミビル併用療法の治療的効果 kn-title=Combined effect of anti-high-mobility group box-1 monoclonal antibody and peramivir against influenza A virus-induced pneumonia in mice en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=HatayamaKazuki en-aut-sei=Hatayama en-aut-mei=Kazuki kn-aut-name=畑山一貴 kn-aut-sei=畑山 kn-aut-mei=一貴 aut-affil-num=1 ORCID= affil-num=1 en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil=岡山大学大学院医歯薬学総合研究科 END start-ver=1.4 cd-journal=joma no-vol=72 cd-vols= no-issue=4 article-no= start-page=401 end-page=406 dt-received= dt-revised= dt-accepted= dt-pub-year=2018 dt-pub=201808 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mixed HCV Infection of Genotype 1B and Other Genotypes Influences Non-response during Daclatasvir + Asunaprevir Combination Therapy en-subtitle= kn-subtitle= en-abstract= kn-abstract= Daclatasvir (DCV) + asunaprevir (ASV) combination therapy has become available for patients with hepatitis C virus (HCV) serogroup 1 infection. We studied the efficacy of this therapy by focusing on the factors associated with sustained virological responses (SVR) including resistance-associated variants (RAVs) and mixed infection of different HCV genotypes. We enrolled 951 HCV serogroup 1-positive patients who received this combination therapy at our hospital or affiliated hospitals. The presence of RAVs in non-structural (NS) regions 3 and 5A was analyzed by direct sequencing. HCV genotypes were determined by PCR with genotype-specific primers targeting HCV core and NS5B regions. SVR was achieved in 91.1% of patients. Female sex, age > 70 years, and RAVs were significantly associated with non-SVR (p<0.01 for all). Propensity score-matching results among the patients without RAVs regarding sex, age, and fibrosis revealed that mixed HCV infection determined by HCV NS5B genotyping showed significantly lower SVR rates than 1B-mono infection (p=0.02). Female sex and RAVs were significant factors associated with treatment failure of this combination therapy for patients with HCV serogroup 1 infection. Mixed HCV infection other than 1B-mono infection would be useful for predicting treatment failure. en-copyright= kn-copyright= en-aut-name=WadaNozomu en-aut-sei=Wada en-aut-mei=Nozomu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MoriChizuru en-aut-sei=Mori en-aut-mei=Chizuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakaguchiKoichi en-aut-sei=Takaguchi en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujiokaShin-ichi en-aut-sei=Fujioka en-aut-mei=Shin-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KobashiHaruhiko en-aut-sei=Kobashi en-aut-mei=Haruhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MorimotoYoichi en-aut-sei=Morimoto en-aut-mei=Yoichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KariyamaKazuya en-aut-sei=Kariyama en-aut-mei=Kazuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SakaguchiKosaku en-aut-sei=Sakaguchi en-aut-mei=Kosaku kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HashimotoNoriaki en-aut-sei=Hashimoto en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MoriyaAkio en-aut-sei=Moriya en-aut-mei=Akio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KawaguchiMitsuhiko en-aut-sei=Kawaguchi en-aut-mei=Mitsuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MiyatakeHirokazu en-aut-sei=Miyatake en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=HagiharaHiroaki en-aut-sei=Hagihara en-aut-mei=Hiroaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=KubotaJunichi en-aut-sei=Kubota en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=TakayamaHiroki en-aut-sei=Takayama en-aut-mei=Hiroki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=TakeuchiYasuto en-aut-sei=Takeuchi en-aut-mei=Yasuto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=YasunakaTetsuya en-aut-sei=Yasunaka en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=OkadaHiroyuki en-aut-sei=Okada en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= affil-num=1 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital kn-affil= affil-num=5 en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital kn-affil= affil-num=6 en-affil=Department of Internal Medicine, Okayama Red Cross Hospital kn-affil= affil-num=7 en-affil=Department of Gastroenterology and Hepatology, Kurashiki Central Hospital kn-affil= affil-num=8 en-affil=Department of Liver Disease Center, Okayama City Hospital kn-affil= affil-num=9 en-affil=Department of Internal Medicine, Fukuyama City Hospital kn-affil= affil-num=10 en-affil=Department of Internal Medicine, Mihara Red Cross Hospital kn-affil= affil-num=11 en-affil=Department of Gastroenterology, Mitoyo General Hospital kn-affil= affil-num=12 en-affil=Department of Internal Medicine, Kawaguchi Medical Clinic kn-affil= affil-num=13 en-affil=Department of Internal Medicine, Hiroshima City Hospital kn-affil= affil-num=14 en-affil=Department of Gastroenterology, Sumitomo Besshi Hospital kn-affil= affil-num=15 en-affil=Department of Internal Medicine, Tajiri Hospital kn-affil= affil-num=16 en-affil=Department of Gastroenterology, Tsuyama Central Hospital kn-affil= affil-num=17 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=18 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=19 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=20 en-affil=Health Service Center, Okayama University kn-affil= affil-num=21 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=mixed genotype kn-keyword=mixed genotype en-keyword=daclatasvir kn-keyword=daclatasvir en-keyword=asunaprevir kn-keyword=asunaprevir en-keyword=HCV kn-keyword=HCV en-keyword= serogrouping 1 infection kn-keyword= serogrouping 1 infection END start-ver=1.4 cd-journal=joma no-vol=9 cd-vols= no-issue=12 article-no= start-page=371 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=20171204 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Characterization of a Novel Bat Adenovirus Isolated from Straw-Colored Fruit Bat (Eidolon helvum). en-subtitle= kn-subtitle= en-abstract= kn-abstract= Bats are important reservoirs for emerging zoonotic viruses. For extensive surveys of potential pathogens in straw-colored fruit bats (Eidolon helvum) in Zambia, a total of 107 spleen samples of E. helvum in 2006 were inoculated onto Vero E6 cells. The cell culture inoculated with one of the samples (ZFB06-106) exhibited remarkable cytopathic changes. Based on the ultrastructural property in negative staining and cross-reactivity in immunofluorescence assays, the virus was suspected to be an adenovirus, and tentatively named E. helvum adenovirus 06-106 (EhAdV 06-106). Analysis of the full-length genome of 30,134 bp, determined by next-generation sequencing, showed the presence of 28 open reading frames. Phylogenetic analyses confirmed that EhAdV 06-106 represented a novel bat adenovirus species in the genus Mastadenovirus. The virus shared similar characteristics of low G + C contents with recently isolated members of species Bat mastadenoviruses E, F and G, from which EhAdV 06-106 diverged by more than 15% based on the distance matrix analysis of DNA polymerase amino acid sequences. According to the taxonomic criteria, we propose the tentative new species name "Bat mastadenovirus H". Because EhAdV 06-106 exhibited a wide in vitro cell tropism, the virus might have a potential risk as an emerging virus through cross-species transmission. en-copyright= kn-copyright= en-aut-name=OgawaHirohito en-aut-sei=Ogawa en-aut-mei=Hirohito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KajiharaMasahiro en-aut-sei=Kajihara en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NaoNaganori en-aut-sei=Nao en-aut-mei=Naganori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ShigenoAsako en-aut-sei=Shigeno en-aut-mei=Asako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujikuraDaisuke en-aut-sei=Fujikura en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Hang’ombeBernard M. en-aut-sei=Hang’ombe en-aut-mei=Bernard M. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MweeneAaron S. en-aut-sei=Mweene en-aut-mei=Aaron S. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MutemwaAlisheke en-aut-sei=Mutemwa en-aut-mei=Alisheke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SquarreDavid en-aut-sei=Squarre en-aut-mei=David kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=HigashiHideaki en-aut-sei=Higashi en-aut-mei=Hideaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=SawaHirofumi en-aut-sei=Sawa en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=TakadaAyato en-aut-sei=Takada en-aut-mei=Ayato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil= Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=3 en-affil= Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=4 en-affil= Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=5 en-affil=Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=6 en-affil=Department of Paraclinical Studies, School of Veterinary Medicine, University of Zambia kn-affil= affil-num=7 en-affil=Department of Disease Control, School of Veterinary Medicine, University of Zambia kn-affil= affil-num=8 en-affil= Provincial Veterinary Office, Department of Veterinary Services, Ministry of Fisheries and Livestock kn-affil= affil-num=9 en-affil=Department of National Parks and Wildlife, Ministry of Tourism and Arts kn-affil= affil-num=10 en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=12 en-affil= Division of Molecular Pathobiology, Research Center for Zoonosis Control, Hokkaido University kn-affil= affil-num=13 en-affil=Global Institution for Collaborative Research and Education (GI-CoRE), Hokkaido University kn-affil= en-keyword=Eidolon helvum kn-keyword=Eidolon helvum en-keyword=Zambia kn-keyword=Zambia en-keyword=adenovirus kn-keyword=adenovirus en-keyword=bat kn-keyword=bat END start-ver=1.4 cd-journal=joma no-vol=93 cd-vols= no-issue=7 article-no= start-page=1422 end-page=1431 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201207 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Development of hepatitis C virus production reporter-assay systems using two different hepatoma cell lines en-subtitle= kn-subtitle= en-abstract= kn-abstract=　A hepatitis C virus (HCV) infection system was developed previously using the HCV JFH-1 strain (genotype 2a) and HuH-7 cells, and this cell culture is so far the only robust production system for HCV. In patients with chronic hepatitis C, the virological effects of pegylated interferon and ribavirin therapy differ depending on the HCV strain and the genetic background of the host. Recently, we reported the hepatoma-derived Li23 cell line, in which the JFH-1 life cycle is reproduced at a level almost equal to that in HuH-7-derived RSc cells. To monitor the HCV life cycle more easily, we here developed JFH-1 reporter-assay systems using both HuH-7- and Li23-derived cell lines. To identify any genetic mutations by long-term cell culture, HCV RNAs in HuH-7 cells were amplified 130 days after infection and subjected to sequence analysis to find adaptive mutation(s) for robust virus replication. We identified two mutations, H2505Q and V2995L, in the NS5B region. V2995L but not H2505Q enhanced JFH-1 RNA replication. However, we found that H2505Q but not V2995L enhanced HCV RNA replication of strain O (genotype 1b). We also selected highly permissive D7 cells by serial subcloning of Li23 cells. The expression levels of claudin-1 and Niemann-Pick C1-like 1 in D7 cells are higher than those in parental Li23 cells. In this study, we developed HCV JFH-1 reporter-assay systems using two distinct hepatoma cell lines, HuH-7 and Li23. The mutations in NS5B resulted in different effects on strains O and JFH-1 HCV RNA replication. en-copyright= kn-copyright= en-aut-name=TakedaMidori en-aut-sei=Takeda en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Department of Tumor Virology, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Tumor Virology, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Tumor Virology, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Virology II, National Institute of Infectious Disease kn-affil= affil-num=5 en-affil=Department of Tumor Virology, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= END start-ver=1.4 cd-journal=joma no-vol=167 cd-vols= no-issue=1 article-no= start-page=74 end-page=85 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201207 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Identification of host genes showing differential expression profiles with cell-based long-term replication of hepatitis C virus RNA en-subtitle= kn-subtitle= en-abstract= kn-abstract=　Persistent hepatitis C virus (HCV) infection frequently causes hepatocellular carcinoma. However, the mechanisms of HCV-associated hepatocarcinogenesis and disease progression are unclear. Although the human hepatoma cell line, HuH-7, has been widely used as the only cell culture system for robust HCV replication, we recently developed new human hepatoma Li23 cell line-derived OL, OL8, OL11, and OL14 cells, in which genome-length HCV RNA (O strain of genotype 1b) efficiently replicates. OL, OL8, OL11, and OL14 cells were cultured for more than 2 years. We prepared cured cells from OL8 and OL11 cells by interferon-γ treatment. The cured cells were also cultured for more than 2 years. cDNA microarray and RT-PCR analyses were performed using total RNAs prepared from these cells. We first selected several hundred highly or moderately expressed probes, the expression levels of which were upregulated or downregulated at ratios of more than 2 or less than 0.5 in each set of compared cells (e.g., parent OL8 cells versus OL8 cells cultured for 2 years). From among these probes, we next selected those whose expression levels commonly changed during a 2-year culture of genome-length HCV RNA-replicating cells, but which did not change during a 2-year culture period in cured cells. We further examined the expression levels of the selected candidate genes by RT-PCR analysis using additional specimens from the cells cultured for 3.5 years. Reproducibility of the RT-PCR analysis using specimens from recultured cells was also confirmed. Finally, we identified 5 upregulated genes and 4 downregulated genes, the expression levels of which were irreversibly altered during 3.5-year replication of HCV RNA. These genes may play roles in the optimization of the environment in HCV RNA replication, or may play key roles in the progression of HCV-associated hepatic diseases. en-copyright= kn-copyright= en-aut-name=SejimaHiroe en-aut-sei=Sejima en-aut-mei=Hiroe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MoriKyoko en-aut-sei=Mori en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= en-keyword=HCV kn-keyword=HCV en-keyword=HCV RNA replication system kn-keyword=HCV RNA replication system en-keyword=Li23 cells kn-keyword=Li23 cells en-keyword=Long-term RNA replication kn-keyword=Long-term RNA replication en-keyword=Upregulated host genes kn-keyword=Upregulated host genes en-keyword=Downregulated host genes kn-keyword=Downregulated host genes END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=20170324 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=突発性発疹患児の急性期から回復期における唾液中ヒトヘルペスウイルス-6および-7DNAのモニタリング kn-title=Monitoring of Human Herpesviruses-6 and -7 DNA in Saliva Samples During the Acute and Convalescent Phases of Exanthem Subitum en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MiyazakiYuki en-aut-sei=Miyazaki en-aut-mei=Yuki kn-aut-name=宮崎裕樹 kn-aut-sei=宮崎 kn-aut-mei=裕樹 aut-affil-num=1 ORCID= affil-num=1 en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil=岡山大学大学医歯薬学総合研究科 END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=2 article-no= start-page=99 end-page=102 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20160801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 2015 Incentive Award of the Okayama Medical Association in Cancer Research (2015 Hayashibara Prize and Yamada Prize) kn-title=平成27年度岡山医学会賞 がん研究奨励賞（林原賞・山田賞） en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name=團迫浩方 kn-aut-sei=團迫 kn-aut-mei=浩方 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=2 article-no= start-page=91 end-page=94 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20160801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 2015 Incentive Award of the Okayama Medical Association in General Medical Science (2015 Yuuki Prize) kn-title=平成27年度岡山医学会賞 総合研究奨励賞（結城賞） en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KajitaAi en-aut-sei=Kajita en-aut-mei=Ai kn-aut-name=梶田藍 kn-aut-sei=梶田 kn-aut-mei=藍 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Dermatology, Okayama University Hospital kn-affil=岡山大学病院　皮膚科 END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=2 article-no= start-page=111 end-page=118 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201604 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Rab13 Is Involved in the Entry Step of Hepatitis C Virus Infection en-subtitle= kn-subtitle= en-abstract= kn-abstract=Membrane transport probably participates in the lifecycle of hepatitis C virus (HCV). Rab proteins are essential host factors for HCV RNA replication, but these proteins’ roles in other steps of the HCV lifecycle are not clear. The tight junction (TJ) plays a key role in HCV infection. Rab13 regulates the endocytic recycling of the TJ-associated proteins. Here we investigated whether Rab13 is involved in the HCV entry step. We used HuH-7-derived RSc cells and Li23-derived D7 cells. To evaluate the effect of Rab13 in HCV infection, we transfected the cells with siRNA targeting Rab13 before HCV infection. The down-regulation of Rab13 inhibited HCV infection. The D7 cells had showed a greater inhibitory effect against HCV infection compared to that in the RSc cells by Rab13 knockdown. Next, to evaluate the effect of Rab13 after infection, we inoculated the cells with HCV before transfection of the siRNA. The down-regulation of Rab13 did not show any effects after HCV infection. We further examined whether Rab13 would influence HCV RNA replication by using HCV replicon-harboring cells. The results revealed that Rab13 did not affect the step of HCV RNA replication. These results suggest that Rab13 plays an important role in the step of HCV entry. en-copyright= kn-copyright= en-aut-name=TakedaMidori en-aut-sei=Takeda en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SatohShinya en-aut-sei=Satoh en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Virology II, National Institute of Infectious Diseases affil-num=6 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=hepatitis C virus kn-keyword=hepatitis C virus en-keyword=Rab13 kn-keyword=Rab13 en-keyword=occludin kn-keyword=occludin en-keyword=claudin 1 kn-keyword=claudin 1 END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=2 article-no= start-page=75 end-page=88 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201604 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Molecular Mechanism Underlying the Suppression of CPB2 Expression Caused by Persistent Hepatitis C Virus RNA Replication en-subtitle= kn-subtitle= en-abstract= kn-abstract=The mechanisms of hepatitis C virus (HCV)-associated hepatocarcinogenesis and disease progression are unclear. We previously observed that the expression level of carboxypeptidase B2 (CPB2) gene was remarkably suppressed by persistent HCV RNA replication in human hepatoma cell line Li23-derived cells. The results of the present study demonstrated that the CPB2 expression in patients with chronic hepatitis C was inversely correlated with several risk factors of hepatic fibrosis or steatosis, although ectopic CPB2 expression did not suppress the expression of fibrogenic or lipogenic genes. The suppressed CPB2 expression was restored by treatment with 5-azacytidine. To clarify the mechanism underlying this phenomenon, we analyzed the CPB2 promoter, and the results revealed that (1) hepatocyte nuclear factor 1 (HNF1), especially HNF1α, was essential for the CPB2 promoter, and (2) CPB2 promoter was not methylated by persistent HCV RNA replication. The expression levels of HNF1α and HNF1β were also not changed by persistent HCV RNA replication. These results suggest the existence of 5-azacytidine-inducible or -reducible unknown factor(s) that can control the CPB2 expression. To evaluate this idea we performed a microarray analysis, and several gene candidates corresponding to the suggested factor(s) were identified. en-copyright= kn-copyright= en-aut-name=SejimaHiroe en-aut-sei=Sejima en-aut-mei=Hiroe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SatohShinya en-aut-sei=Satoh en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HondaMasao en-aut-sei=Honda en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KanekoShuichi en-aut-sei=Kaneko en-aut-mei=Shuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Gastroenterology, Kanazawa University Graduate School of Medicine affil-num=5 en-affil= kn-affil=Department of Gastroenterology, Kanazawa University Graduate School of Medicine affil-num=6 en-affil= kn-affil=Department of Persistent and Oncogenic Viruses, Kagoshima University Graduate School of Medical and Dental Sciences affil-num=7 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=persistent hepatitis C virus replication kn-keyword=persistent hepatitis C virus replication en-keyword=carboxypeptidase B2 kn-keyword=carboxypeptidase B2 en-keyword=suppression mechanism of CPB2 expression kn-keyword=suppression mechanism of CPB2 expression en-keyword=DNA methylation kn-keyword=DNA methylation en-keyword=hepatocyte nuclear factor 1 kn-keyword=hepatocyte nuclear factor 1 END start-ver=1.4 cd-journal=joma no-vol=9 cd-vols= no-issue=3 article-no= start-page=e91156 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140313 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Genetic Characterization of Hepatitis C Virus in Long-Term RNA Replication Using Li23 Cell Culture Systems en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background　 　 The most distinguishing genetic feature of hepatitis C virus (HCV) is its remarkable diversity and variation. To understand this feature, we previously performed genetic analysis of HCV in the long-term culture of human hepatoma HuH-7-derived HCV RNA-replicating cell lines. On the other hand, we newly established HCV RNA-replicating cell lines using human hepatoma Li23 cells, which were distinct from HuH-7 cells. 　 Methodology/Principal Findings　 　 Li23-derived HCV RNA-replicating cells were cultured for 4 years. We performed genetic analysis of HCVs recovered from these cells at 0, 2, and 4 years in culture. Most analysis was performed in two separate parts: one part covered from the 5′-terminus to NS2, which is mostly nonessential for RNA replication, and the other part covered from NS3 to NS5B, which is essential for RNA replication. Genetic mutations in both regions accumulated in a time-dependent manner, and the mutation rates in the 5′-terminus-NS2 and NS3-NS5B regions were 4.0?9.0×10?3 and 2.7?4.0×10?3 base substitutions/site/year, respectively. These results suggest that the variation in the NS3-NS5B regions is affected by the pressure of RNA replication. Several in-frame deletions (3?105 nucleotides) were detected in the structural regions of HCV RNAs obtained from 2-year or 4-year cultured cells. Phylogenetic tree analyses clearly showed that the genetic diversity of HCV was expanded in a time-dependent manner. The GC content of HCV RNA was significantly increased in a time-dependent manner, as previously observed in HuH-7-derived cell systems. This phenomenon was partially due to the alterations in codon usages for codon optimization in human cells. Furthermore, we demonstrated that these long-term cultured cells were useful as a source for the selection of HCV clones showing resistance to anti-HCV agents. 　 Conclusions/Significance　 　 Long-term cultured HCV RNA-replicating cells are useful for the analysis of evolutionary dynamics and variations of HCV and for drug-resistance analysis. en-copyright= kn-copyright= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SejimaHiroe en-aut-sei=Sejima en-aut-mei=Hiroe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UedaYouki en-aut-sei=Ueda en-aut-mei=Youki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MoriKyoko en-aut-sei=Mori en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SatohShinya en-aut-sei=Satoh en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=8 cd-vols= no-issue=8 article-no= start-page=e72519 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130830 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=New Preclinical Antimalarial Drugs Potently Inhibit Hepatitis C Virus Genotype 1b RNA Replication en-subtitle= kn-subtitle= en-abstract= kn-abstract=BACKGROUND: Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. Although new triple therapy (pegylated-interferon, ribavirin, and telaprevir/boceprevir) has recently been started and is expected to achieve a sustained virologic response of more than 70% in HCV genotype 1 patients, there are several problems to be resolved, including skin rash/ageusia and advanced anemia. Thus a new type of anti-HCV drug is still needed. 　 METHODOLOGY/PRINCIPAL FINDINGS: 　 　 Recently developed HCV drug assay systems using HCV-RNA-replicating cells (e.g., HuH-7-derived OR6 and Li23-derived ORL8) were used to evaluate the anti-HCV activity of drug candidates. During the course of the evaluation of anti-HCV candidates, we unexpectedly found that two preclinical antimalarial drugs (N-89 and its derivative N-251) showed potent anti-HCV activities at tens of nanomolar concentrations irrespective of the cell lines and HCV strains of genotype 1b. We confirmed that replication of authentic HCV-RNA was inhibited by these drugs. Interestingly, however, this anti-HCV activity did not work for JFH-1 strain of genotype 2a. We demonstrated that HCV-RNA-replicating cells were cured by treatment with only N-89. A comparative time course assay using N-89 and interferon-α demonstrated that N-89-treated ORL8 cells had more rapid anti-HCV kinetics than did interferon-α-treated cells. This anti-HCV activity was largely canceled by vitamin E. In combination with interferon-α and/or ribavirin, N-89 or N-251 exhibited a synergistic inhibitory effect.　 　 CONCLUSIONS/SIGNIFICANCE:　 　 We found that the preclinical antimalarial drugs N-89 and N-251 exhibited very fast and potent anti-HCV activities using cell-based HCV-RNA-replication assay systems. N-89 and N-251 may be useful as a new type of anti-HCV reagents when used singly or in combination with interferon and/or ribavirin. en-copyright= kn-copyright= en-aut-name=UedaYouki en-aut-sei=Ueda en-aut-mei=Youki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakedaMidori en-aut-sei=Takeda en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MoriKyoko en-aut-sei=Mori en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KimHye-Sook en-aut-sei=Kim en-aut-mei=Hye-Sook kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SatoAkira en-aut-sei=Sato en-aut-mei=Akira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=WatayaYusuke en-aut-sei=Wataya en-aut-mei=Yusuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Virology II, National Institute of Infectious Disease affil-num=6 en-affil= kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University affil-num=7 en-affil= kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University affil-num=8 en-affil= kn-affil=Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Okayama University affil-num=9 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=127 cd-vols= no-issue=3 article-no= start-page=261 end-page=262 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=20151201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 56th Annual Meeting of the Japanese Society for Clinical Virology kn-title=第56回日本臨床ウイルス学会開催報告 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name=山田雅夫 kn-aut-sei=山田 kn-aut-mei=雅夫 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=5 article-no= start-page=279 end-page=290 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201510 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Inhibitory Effects of Edaravone, a Free Radical Scavenger, on Cytokine-induced Hyperpermeability of Human Pulmonary Microvascular Endothelial Cells:A Comparison with Dexamethasone and Nitric Oxide Synthase Inhibitor en-subtitle= kn-subtitle= en-abstract= kn-abstract=Lung hyperpermeability affects the development of acute respiratory distress syndrome (ARDS), but therapeutic strategies for the control of microvascular permeability have not been established. We examined the effects of edaravone, dexamethasone, and N-monomethyl-L-arginine (L-NMMA) on permeability changes in human pulmonary microvascular endothelial cells (PMVEC) under a hypercytokinemic state. Human PMVEC were seeded in a Boyden chamber. After monolayer confluence was achieved, the culture media were replaced respectively by culture media containing edaravone, dexamethasone, and L-NMMA. After 24-h incubation, the monolayer was stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Fluorescein-labeled dextran was added. Then the trans-human PMVEC leak was measured. Expressions of vascular endothelial-cadherin (VE-cadherin) and zonula occludens-1 protein (ZO-1) were evaluated using real-time quantitative polymerase chain reaction and immunofluorescence microscopy. The results showed that TNF-α＋IL-1β markedly increased pulmonary microvascular permeability. Pretreatment with edaravone, dexamethasone, or L-NMMA attenuated the hyperpermeability and inhibited the cytokine-induced reduction of VE-cadherin expression on immunofluorescence staining. Edaravone and dexamethasone increased the expression of ZO-1 at both the mRNA and protein levels. Edaravone and dexamethasone inhibited the permeability changes of human PMVEC, at least partly through an enhancement of VE-cadherin. Collectively, these results suggest a potential therapeutic approach for intervention in patients with ARDS. en-copyright= kn-copyright= en-aut-name=SaitoYukie en-aut-sei=Saito en-aut-mei=Yukie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FujiiYousuke en-aut-sei=Fujii en-aut-mei=Yousuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YashiroMasato en-aut-sei=Yashiro en-aut-mei=Masato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsugeMitsuru en-aut-sei=Tsuge en-aut-mei=Mitsuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NosakaNobuyuki en-aut-sei=Nosaka en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=YamadaMutsuko en-aut-sei=Yamada en-aut-mei=Mutsuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TsukaharaHirokazu en-aut-sei=Tsukahara en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MorishimaTsuneo en-aut-sei=Morishima en-aut-mei=Tsuneo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=pulmonary microvascular endothelial cells kn-keyword=pulmonary microvascular endothelial cells en-keyword=permeability kn-keyword=permeability en-keyword=edaravone kn-keyword=edaravone en-keyword=vascular endothelial-cadherin kn-keyword=vascular endothelial-cadherin en-keyword=zonula occludens-1 protein kn-keyword=zonula occludens-1 protein END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=2015 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The cyclic GMP-AMP synthetase-STING signaling pathway is required for both the innate immune response against HBV and the suppression of HBV assembly en-subtitle= kn-subtitle= en-abstract= kn-abstract=During viral replication, the innate immune response is induced through the recognition of viral replication intermediates by host factor(s). One of these host factors, cyclic GMP-AMP synthetase (cGAS), was recently reported to be involved in the recognition of viral DNA derived from DNA viruses. However, it is uncertain whether cGAS is involved in the recognition of hepatitis B virus (HBV), which is a hepatotropic DNA virus. In the present study, we demonstrated that HBV genome-derived dsDNA induced the innate immune response through cGAS and its adaptor protein, STING, in human hepatoma Li23 cells expressing high levels of cGAS. In addition, we demonstrated that HBV infection induced ISG56 through the cGAS-STING signaling pathway. This signaling pathway also showed an antiviral response towards HBV through the suppression of viral assembly. From these results, we conclude that the cGAS-STING signaling pathway is required for not only the innate immune response against HBV but also the suppression of HBV assembly. The cGAS-STING signaling pathway may thus be a novel target for anti-HBV strategies. en-copyright= kn-copyright= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UedaYouki en-aut-sei=Ueda en-aut-mei=Youki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OkumuraNobuaki en-aut-sei=Okumura en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SatohShinya en-aut-sei=Satoh en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SugiyamaMasaya en-aut-sei=Sugiyama en-aut-mei=Masaya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MizokamiMasashi en-aut-sei=Mizokami en-aut-mei=Masashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine affil-num=6 en-affil= kn-affil=Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine affil-num=7 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry affil-num=8 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=Antiviral response kn-keyword=Antiviral response en-keyword=hepatitis B virus kn-keyword=hepatitis B virus en-keyword=innate immune response kn-keyword=innate immune response en-keyword=cGAS-STING signaling pathway kn-keyword=cGAS-STING signaling pathway en-keyword=viral assembly kn-keyword=viral assembly END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=4 article-no= start-page=237 end-page=244 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201508 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effectiveness of Extending Treatment Duration in Therapy with Pegylated Interferon and Ribavirin for Genotype 2 Hepatitis C Virus Infection en-subtitle= kn-subtitle= en-abstract= kn-abstract=The effectiveness of extending treatment duration as response guided therapy was previously reported for chronic hepatitis C (CHC) genotype 1, but is still controversial for genotype 2. The present study is a retrospective cohort study to investigate the effectiveness of extending treatment duration in therapy with pegylated interferon and ribavirin for patients with CHC genotype 2 by focusing on the timing at which patients obtained undetectable HCV RNA. A total of 306 patients who obtained undetectable HCV RNA by week 24 of treatment and completed 24 weeks of treatment were enrolled. Rapid virological response (RVR) to standard therapy was achieved by 122 patients (51ｵ), and 89ｵ of them obtained sustained virological response (SVR), while 69ｵ of non-RVR patients achieved SVR. Non-RVR patients with undetectable HCV RNA at week 8, and insufficient adherence＜80ｵ pegylated interferon and ribavirin during the first 24 weeks, significantly improved their SVR rate by extended therapy. Among patients receiving extended therapy, drug adherences did not differ between SVR and non-SVR patients, indicating that extending treatment duration might compensate for insufficient antiviral effects due to insufficient drug adherences. This finding might be useful in creating a guideline for extending treatment duration for patients with CHC genotype 2. en-copyright= kn-copyright= en-aut-name=NanbaShintarou en-aut-sei=Nanba en-aut-mei=Shintarou kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FujiokaShin-ichi en-aut-sei=Fujioka en-aut-mei=Shin-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ArakiYasuyuki en-aut-sei=Araki en-aut-mei=Yasuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakaguchiKouichi en-aut-sei=Takaguchi en-aut-mei=Kouichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HashimotoNoriaki en-aut-sei=Hashimoto en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SekiHiroyuki en-aut-sei=Seki en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=2 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=3 en-affil= kn-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital affil-num=4 en-affil= kn-affil=Department of Internal Medicine, Hiroshima City Hospital affil-num=5 en-affil= kn-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital affil-num=6 en-affil= kn-affil=Department of Internal Medicine, Mihara Red Cross Hospital affil-num=7 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=8 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University affil-num=9 en-affil= kn-affil=Health Service Center, Okayama University affil-num=10 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University en-keyword=hepatitis C virus kn-keyword=hepatitis C virus en-keyword=interferon kn-keyword=interferon en-keyword=genotype 2 kn-keyword=genotype 2 en-keyword=response-guided therapy kn-keyword=response-guided therapy END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=2 article-no= start-page=71 end-page=78 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201504 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Annexin A1 Negatively Regulates Viral RNA Replication of Hepatitis C Virus en-subtitle= kn-subtitle= en-abstract= kn-abstract=Persistent infection with hepatitis C virus (HCV) often causes chronic hepatitis, and then shows a high rate of progression to liver cirrhosis and hepatocellular carcinoma. To clarify the mechanism of the persistent HCV infection is considered to be important for the discovery of new target(s) for the development of anti-HCV strategies. In the present study, we found that the expression level of annexin A1 (ANXA1) in human hepatoma cell line Li23-derived D7 cells was remarkably lower than that in parental Li23 cells, whereas the susceptibility of D7 cells to HCV infection was much higher than that of Li23 cells. Therefore, we hypothesized that ANXA1 negatively regulates persistent HCV infection through the inhibition of viral RNA replication. The results revealed that HCV production was significantly inhibited without a concomitant reduction in the amount of lipid droplets in the D7 cells stably expressing exogenous ANXA1. Further, we demonstrated that ANXA1 negatively regulated the step of viral RNA replication rather than that of viral entry in human hepatocytes. These results suggest that ANXA1 would be a novel target for the development of anti-HCV strategies. en-copyright= kn-copyright= en-aut-name=HiramotoHiroki en-aut-sei=Hiramoto en-aut-mei=Hiroki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakedaMidori en-aut-sei=Takeda en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SatohShinya en-aut-sei=Satoh en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Virology II, National Institute of Infectious Disease affil-num=6 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=HCV kn-keyword=HCV en-keyword=annexin A1 kn-keyword=annexin A1 en-keyword=Li23 cell line kn-keyword=Li23 cell line en-keyword=Li23-derived D7 cells kn-keyword=Li23-derived D7 cells en-keyword=HCV-JFH-1 kn-keyword=HCV-JFH-1 END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=5 article-no= start-page=291 end-page=302 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Hepatitis C Virus-specific T-cell Response Correlates with Hepatitis Activity and Donor IL28B Genotype Early after Liver Transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract=It is not known how the immune system targets hepatitis C virus (HCV)-infected HLA-mismatched hepatocytes under immune-suppressed conditions after orthotopic liver transplantation (OLT). In addition, the relationship between the HCV-specific immune response and IL28B variants as predictors of HCV clearance has not been well-characterized. We determined the IL28B polymorphisms for 57 post-OLT HCV carriers, and we assessed the HCV-specific immune responses by measuring the peripheral blood mononuclear cell-derived HCV-specific interferon-gamma (IFN-γ) response using an enzyme-linked immunospot assay. At 1-3 years after OLT, patients with no active hepatitis showed higher total spots on the immunospot assay. At＞3 years after OLT, patients with resolved HCV showed higher levels of core, NS3, NS5A, and total spots compared to the chronic hepatitis patients. The IL28B major genotype in the donors correlated with higher spot counts for NS5A and NS5B proteins at 1-3 years after OLT. In the post-OLT setting, the HCV-specific immune response could be strongly induced in patients with no active hepatitis with an IL28B major donor or sustained virological response. Strong immune responses in the patients with no active hepatitis could only be maintained for 3 years and diminished later. It may be beneficial to administer IFN treatment starting 3 years after OLT, to induce the maximum immunological effect. en-copyright= kn-copyright= en-aut-name=TsuzakiRyuichiro en-aut-sei=Tsuzaki en-aut-mei=Ryuichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YagiTakahito en-aut-sei=Yagi en-aut-mei=Takahito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KoikeKazuko en-aut-sei=Koike en-aut-mei=Kazuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShirahaHidenori en-aut-sei=Shiraha en-aut-mei=Hidenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MiyakeYasuhiro en-aut-sei=Miyake en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=SadamoriHiroshi en-aut-sei=Sadamori en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=ShinouraSusumu en-aut-sei=Shinoura en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=UmedaYuzo en-aut-sei=Umeda en-aut-mei=Yuzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=YoshidaRyuichi en-aut-sei=Yoshida en-aut-mei=Ryuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=NobuokaDaisuke en-aut-sei=Nobuoka en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=UtsumiMasashi en-aut-sei=Utsumi en-aut-mei=Masashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=NakayamaEiichi en-aut-sei=Nakayama en-aut-mei=Eiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=FujiwaraToshiyoshi en-aut-sei=Fujiwara en-aut-mei=Toshiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= affil-num=1 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Health Service Center, Okayama University affil-num=7 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=12 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=13 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=14 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=15 en-affil= kn-affil=Kawasaki University of Medical Welfare affil-num=16 en-affil= kn-affil=Department of Gastroenterological Surgery Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=17 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=interferon gamma kn-keyword=interferon gamma en-keyword=ELISPOT assay kn-keyword=ELISPOT assay en-keyword=single nucleotide polymorphisms kn-keyword=single nucleotide polymorphisms en-keyword=dendritic cell kn-keyword=dendritic cell en-keyword=CD4 T cell kn-keyword=CD4 T cell END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=5 article-no= start-page=263 end-page=268 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Nursing Support Increases the Efficacy of Interferon Therapy in Patients with Chronic Hepatitis C en-subtitle= kn-subtitle= en-abstract= kn-abstract=Nursing support might help patients with chronic hepatitis C (CHC) remain in good mental and physical condition during interferon (IFN) therapy. However, the effects of nursing support have not been studied adequately in this context. This case-control study evaluated the effects of nursing support during IFN therapy. Twenty-four CHC patients who received pegylated IFN and ribavirin were enrolled. Nurses advised patients on the maintenance of their mental and physical condition at weekly visits, based on the results of written questionnaires. An additional 24 patients who received IFN therapy without nursing support and who were matched for age, sex, platelet count, viral serogroup and IFN regimen were selected with propensity score matching as controls. The patients with nursing support during IFN therapy achieved higher sustained virological responses (79%) than those without nursing support (58%). Adherence to the IFN and ribavirin regimens at 24 weeks of therapy were slightly higher in the patients with nursing support than those without it, but these differences were not statistically significant. Adherence to ribavirin after 24 weeks of therapy was significantly higher in those with nursing support than those without it (93% and 66%, p＝0.045). These results suggested that nursing support services could contribute to the virological responses of CHC patients by promoting drug-regimen adherence. en-copyright= kn-copyright= en-aut-name=NambaShihoko en-aut-sei=Namba en-aut-mei=Shihoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyakeKayoko en-aut-sei=Miyake en-aut-mei=Kayoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HazamaTomoko en-aut-sei=Hazama en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HitobeYu en-aut-sei=Hitobe en-aut-mei=Yu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamasakiNoriko en-aut-sei=Yamasaki en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShirahaHidenori en-aut-sei=Shiraha en-aut-mei=Hidenori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NousoKazuhiro en-aut-sei=Nouso en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Department of Nursing, Okayama University Hospital affil-num=2 en-affil= kn-affil=Department of Nursing, Okayama University Hospital affil-num=3 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Nursing, Okayama University Hospital affil-num=5 en-affil= kn-affil=Department of Nursing, Okayama University Hospital affil-num=6 en-affil= kn-affil=Department of Nursing, Okayama University Hospital affil-num=7 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Health Service Center, Okayama University affil-num=11 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=chronic hepatitis C kn-keyword=chronic hepatitis C en-keyword=nursing support kn-keyword=nursing support en-keyword=interferon therapy kn-keyword=interferon therapy END start-ver=1.4 cd-journal=joma no-vol=29 cd-vols= no-issue=2 article-no= start-page=337 end-page=343 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201402 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Assessment of health-related quality of life and how it predicts the outcome of pegylated interferon and ribavirin therapy for chronic hepatitis C en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background and Aim: Chronic infection with hepatitis C virus (HCV) decreases health-related quality of life (HRQOL). The present study was planned to investigate the impact of HRQOL of patients with chronic hepatitis C (CHC) on the outcomes of therapy with pegylated interferon and ribavirin (RBV), in addition to IL28B polymorphisms. Methods: The present study enrolled 228 CHC patients and assessed their HRQOLs prospectively with the 36-item short-form health survey. Results: The patients with CHC have lower physical HRQOL status than the general population (P = 0.037, the Z-test). The patients with advanced liver diseases exhibited further decreases in HRQOL (P = 0.036, Spearman's rank correlation coefficient). The score of total HRQOL was significantly lower in the group with sustained virological response (SVR) to the therapy with pegylated interferon and RBV than the non-SVR group (P = 0.031, the Mann-Whitney U-test), with significantly lower scores of mental component and its comprising subscales in the SVR group. Stepwise multivariate logistic regression analysis showed that low HRQOL score <= 400 points was significantly associated with SVR (odds ratio = 2.4, P = 0.013), independently from high platelet counts, low HCV RNA, favorable single-nucleotide polymorphism type of IL28B, and HCV serotype 2. The patients with low HRQOL score will have significantly less decrease in HRQOL score by 4 weeks of the treatment than those with high HRQOL score at baseline (P = 0.0045). Conclusion: HRQOL is one of the significant predictor of the outcomes of therapy with pegylated interferon and RBV independently from IL28B polymorphism. en-copyright= kn-copyright= en-aut-name=MatsushitaHiroshi en-aut-sei=Matsushita en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SekiHiroyuki en-aut-sei=Seki en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NanbaShintaro en-aut-sei=Nanba en-aut-mei=Shintaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakeuchiYasuto en-aut-sei=Takeuchi en-aut-mei=Yasuto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MoritouYuki en-aut-sei=Moritou en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YasunakaTetsuya en-aut-sei=Yasunaka en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OnishiHideki en-aut-sei=Onishi en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MiyakeYasuhiro en-aut-sei=Miyake en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=NousoKazuhiro en-aut-sei=Nouso en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Hlth Serv Ctr affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=12 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=13 en-affil= kn-affil=Okayama Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Dent & Pharmaceut Sci en-keyword=HCV kn-keyword=HCV en-keyword=interferon kn-keyword=interferon en-keyword=QOL kn-keyword=QOL END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=1 article-no= start-page=65 end-page=67 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=SFTS : Severe fever with thrombocytopenia syndrome kn-title=重症熱性血小板減少症候群 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=WatanabeTokiko en-aut-sei=Watanabe en-aut-mei=Tokiko kn-aut-name=渡邉都貴子 kn-aut-sei=渡邉 kn-aut-mei=都貴子 aut-affil-num=1 ORCID= en-aut-name=KusanoNobuchika en-aut-sei=Kusano en-aut-mei=Nobuchika kn-aut-name=草野展周 kn-aut-sei=草野 kn-aut-mei=展周 aut-affil-num=2 ORCID= en-aut-name=IwatsukiKeiji en-aut-sei=Iwatsuki en-aut-mei=Keiji kn-aut-name=岩月啓氏 kn-aut-sei=岩月 kn-aut-mei=啓氏 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　感染制御部 affil-num=2 en-affil= kn-affil=岡山大学病院　感染制御部 affil-num=3 en-affil= kn-affil=岡山大学病院　感染制御部 END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=1 article-no= start-page=17 end-page=22 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201402 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Impact of Comorbid Hepatic Steatosis on Treatment of Chronic Hepatitis C in Japanese Patients and the Relationship with Genetic Polymorphism of IL28B, PNPLA3 and LDL Receptor en-subtitle= kn-subtitle= en-abstract= kn-abstract=The impact of hepatic steatosis on interferon therapy for patients with chronic hepatitis C (CHC) has been associated with single-nucleotide polymorphisms (SNP) of IL28B, patatin-like phospholipase domain-containing protein 3 (PNPLA3), and low-density lipoprotein (LDL) receptor. Whether this holds true for Japanese patients, however, remains unresolved. The present study prospectively enrolled 226 Japanese patients with CHC, and investigated the impact of hepatic steatosis and its related SNPs, including rs8099917 of IL28B, rs738409 of PNPLA3, and rs14158 of LDL receptor, on outcomes of peg-interferon and ribavirin therapy. In multivariate logistic regression analysis, significant factors affecting the severity of hepatic steatosis were high body mass index and the minor alleles of IL28B SNP (p＝0.020 and 0.039, respectively). The risk alleles of PNPLA3 SNP also showed weak association (p＝0.059). Severe steatosis and the minor alleles of IL28B SNP were significantly associated with null or partial virological response in patients with HCV genotype 1, as were female gender, and low LDL cholesterol (p＝0.049, and ＜0.001, respectively). The SNP genotype of PNPLA3 and LDL receptor did not have a significant impact on therapeutic outcomes. With respect to the SNP sites examined, the SNP of PNPLA3 has a weak association with severe hepatic steatosis, but not with the outcome of interferon therapy. en-copyright= kn-copyright= en-aut-name=MoritouYuki en-aut-sei=Moritou en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IkedaFusao en-aut-sei=Ikeda en-aut-mei=Fusao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IwasakiYoshiaki en-aut-sei=Iwasaki en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=BabaNobuyuki en-aut-sei=Baba en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakaguchiKouichi en-aut-sei=Takaguchi en-aut-mei=Kouichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SenohTomonori en-aut-sei=Senoh en-aut-mei=Tomonori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NaganoTakuya en-aut-sei=Nagano en-aut-mei=Takuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TakeuchiYasuto en-aut-sei=Takeuchi en-aut-mei=Yasuto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YasunakaTetsuya en-aut-sei=Yasunaka en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=OhnishiHideki en-aut-sei=Ohnishi en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MiyakeYasuhiro en-aut-sei=Miyake en-aut-mei=Yasuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TakakiAkinobu en-aut-sei=Takaki en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=NousoKazuhiro en-aut-sei=Nouso en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= affil-num=1 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Health Service Center, Okayama University affil-num=4 en-affil= kn-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital affil-num=5 en-affil= kn-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital affil-num=6 en-affil= kn-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital affil-num=7 en-affil= kn-affil=Department of Internal Medicine, Kagawa Prefectural Central Hospital affil-num=8 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=12 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=13 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=14 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=hepatic steatosis kn-keyword=hepatic steatosis en-keyword=genetic polymorphism kn-keyword=genetic polymorphism en-keyword=interferon kn-keyword=interferon en-keyword=HCV kn-keyword=HCV END start-ver=1.4 cd-journal=joma no-vol=133 cd-vols= no-issue=9 article-no= start-page=951 end-page=956 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201309 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The engraftment and differentiation of transplanted bone marrow-derived cells in the olfactory bulb after methimazole administration en-subtitle= kn-subtitle= en-abstract= kn-abstract=Conclusion: Bone marrow-derived cells can be engrafted in the olfactory bulb and a few cells can differentiate into mitral/tufted cells in the olfactory bulb. Objectives: To investigate whether bone marrow-derived cells can be engrafted into the olfactory bulb and differentiate into neurons and glial cells after methimazole administration. Methods: Bone marrow of GFP (green fluorescence protein) mice was transplanted into lethally irradiated recipient mice. Immunostaining was performed to confirm the cell types of bone marrow-derived cells expressing GFP. Results: GFP-positive cells were observed in the olfactory bulb at 2 days after methimazole administration. The number of dendritic GFP-positive cells increased up to 30 days after methimazole administration and then decreased. Double immunostaining for GFP and Iba1 or TBX21 showed that a large population of the GFP-positive cells had characteristics of microglia/macrophages and a few cells had characteristics of mitral/tufted cells. en-copyright= kn-copyright= en-aut-name=NodaYohei en-aut-sei=Noda en-aut-mei=Yohei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NishizakiKazunori en-aut-sei=Nishizaki en-aut-mei=Kazunori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshinobuJunko en-aut-sei=Yoshinobu en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OritaYorihisa en-aut-sei=Orita en-aut-mei=Yorihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TsujigiwaHidetsugu en-aut-sei=Tsujigiwa en-aut-mei=Hidetsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Oral Pathol & Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Virol en-keyword=Transplantation kn-keyword=Transplantation en-keyword=regeneration kn-keyword=regeneration en-keyword=olfaction kn-keyword=olfaction en-keyword=mitral cells kn-keyword=mitral cells en-keyword=microglia kn-keyword=microglia END start-ver=1.4 cd-journal=joma no-vol=125 cd-vols= no-issue=2 article-no= start-page=109 end-page=112 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Therapeutic effects of redox-active protein thioredoxin(TRX)-1 in influenza-virus-induced pneumonia in mice kn-title=マウスインフルエンザ肺炎におけるレドックス制御蛋白チオレドキシン（TRX-1）の治療的効果 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=YashiroMasato en-aut-sei=Yashiro en-aut-mei=Masato kn-aut-name=八代将登 kn-aut-sei=八代 kn-aut-mei=将登 aut-affil-num=1 ORCID= en-aut-name=TsukaharaHirokazu en-aut-sei=Tsukahara en-aut-mei=Hirokazu kn-aut-name=塚原宏一 kn-aut-sei=塚原 kn-aut-mei=宏一 aut-affil-num=2 ORCID= en-aut-name=MatsukawaAkihiro en-aut-sei=Matsukawa en-aut-mei=Akihiro kn-aut-name=松川昭博 kn-aut-sei=松川 kn-aut-mei=昭博 aut-affil-num=3 ORCID= en-aut-name=YamadaMutsuko en-aut-sei=Yamada en-aut-mei=Mutsuko kn-aut-name=山田睦子 kn-aut-sei=山田 kn-aut-mei=睦子 aut-affil-num=4 ORCID= en-aut-name=FujiiYosuke en-aut-sei=Fujii en-aut-mei=Yosuke kn-aut-name=藤井洋輔 kn-aut-sei=藤井 kn-aut-mei=洋輔 aut-affil-num=5 ORCID= en-aut-name=NagaokaYoshiharu en-aut-sei=Nagaoka en-aut-mei=Yoshiharu kn-aut-name=長岡義晴 kn-aut-sei=長岡 kn-aut-mei=義晴 aut-affil-num=6 ORCID= en-aut-name=TsugeMitsuru en-aut-sei=Tsuge en-aut-mei=Mitsuru kn-aut-name=津下充 kn-aut-sei=津下 kn-aut-mei=充 aut-affil-num=7 ORCID= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name=山下信子 kn-aut-sei=山下 kn-aut-mei=信子 aut-affil-num=8 ORCID= en-aut-name=ItoToshihiro en-aut-sei=Ito en-aut-mei=Toshihiro kn-aut-name=伊藤利洋 kn-aut-sei=伊藤 kn-aut-mei=利洋 aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name=山田雅夫 kn-aut-sei=山田 kn-aut-mei=雅夫 aut-affil-num=10 ORCID= en-aut-name=MasutaniHiroshi en-aut-sei=Masutani en-aut-mei=Hiroshi kn-aut-name=増谷弘 kn-aut-sei=増谷 kn-aut-mei=弘 aut-affil-num=11 ORCID= en-aut-name=YodoiJunji en-aut-sei=Yodoi en-aut-mei=Junji kn-aut-name=淀井淳司 kn-aut-sei=淀井 kn-aut-mei=淳司 aut-affil-num=12 ORCID= en-aut-name=MorishimaTsuneo en-aut-sei=Morishima en-aut-mei=Tsuneo kn-aut-name=森島恒雄 kn-aut-sei=森島 kn-aut-mei=恒雄 aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（免疫病理） affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=8 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（免疫病理） affil-num=10 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病原ウイルス学 affil-num=11 en-affil= kn-affil=京都大学ウイルス研究所 生体応答学研究部門 affil-num=12 en-affil= kn-affil=京都大学ウイルス研究所 生体応答学研究部門 affil-num=13 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 小児医科学 en-keyword=acute lung injury kn-keyword=acute lung injury en-keyword=cytokine kn-keyword=cytokine en-keyword=influenza virus kn-keyword=influenza virus en-keyword=oxidative stress kn-keyword=oxidative stress en-keyword=thioredoxin-1 kn-keyword=thioredoxin-1 END start-ver=1.4 cd-journal=joma no-vol=41 cd-vols= no-issue=1 article-no= start-page=171 end-page=181 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201301 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Redox-Active Protein Thioredoxin-1 Administration Ameliorates Influenza A Virus (H1N1)-Induced Acute Lung Injury in Mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=Objectives: Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice. Design: Prospective animal trial. Setting: Research laboratory. Subjects: Nine-week-old male C57BL/6 mice inoculated with H1N1. Intervention: The mice were divided into a vehicle-treated group and recombinant human thioredoxin-1-treated group. For survival rate analysis, the vehicle or recombinant human thioredoxin-1 was administered intraperitoneally every second day from day -1 to day 13. For lung lavage and pathological analyses, vehicle or recombinant human thioredoxin-1 was administered intraperitoneally on days 1, 1, and 3. Measurements and Main Results: Lung lavage and pathological analyses were performed at 24, 72, and 120 hrs after inoculation. The recombinant human thioredoxin-1 treatment significantly improved the survival rate of H1N1-inoculated mice, although the treatment did not affect virus propagation in the lung. The treatment significantly attenuated the histological changes and neutrophil infiltration in the lung of H1N1-inoculated mice. The treatment significantly attenuated the production of tumor necrosis factor-a and chemokine (C-X-C motif) ligand 1 in the lung and oxidative stress enhancement, which were observed in H1N1-inoculated mice. H1N1 induced expressions of tumor necrosis factor-a and chemokine (C-X-C motif) ligand 1 in murine lung epithelial cells MLE-12, which were inhibited by the addition of recombinant human thioredoxin-1. The recombinant human thioredoxin-1 treatment started 30 mins after H1N1 inoculation also significantly improved the survival of the mice. Conclusions: Exogenous administration of recombinant human thioredoxin-1 significantly improved the survival rate and attenuated lung histological changes in the murine model of influenza pneumonia. The protective mechanism of thioredoxin-1 might be explained by its potent antioxidative and anti-inflammatory actions. Consequently, recombinant human thioredoxin-1 might be a possible pharmacological strategy for severe influenza virus infection in humans. (Crit Care Med 2013; 41:171-181) en-copyright= kn-copyright= en-aut-name=YashiroMasato en-aut-sei=Yashiro en-aut-mei=Masato kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TsukaharaHirokazu en-aut-sei=Tsukahara en-aut-mei=Hirokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsukawaAkihiro en-aut-sei=Matsukawa en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamadaMutsuko en-aut-sei=Yamada en-aut-mei=Mutsuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujiiYosuke en-aut-sei=Fujii en-aut-mei=Yosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NagaokaYoshiharu en-aut-sei=Nagaoka en-aut-mei=Yoshiharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TsugeMitsuru en-aut-sei=Tsuge en-aut-mei=Mitsuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=ItoToshihiro en-aut-sei=Ito en-aut-mei=Toshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MasutaniHiroshi en-aut-sei=Masutani en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol & Expt Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pediat affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol & Expt Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Virol affil-num=11 en-affil= kn-affil=Kyoto Univ, Inst Virus Res, Dept Biol Responses en-keyword=acute lung injury kn-keyword=acute lung injury en-keyword=cytokine kn-keyword=cytokine en-keyword=influenza virus kn-keyword=influenza virus en-keyword=mouse kn-keyword=mouse en-keyword=oxidative stress kn-keyword=oxidative stress en-keyword=thioredoxin-1 kn-keyword=thioredoxin-1 END start-ver=1.4 cd-journal=joma no-vol=92 cd-vols= no-issue=2 article-no= start-page=361 end-page=369 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201102 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Whole-genome characterization of human group C rotaviruses: identification of two lineages in the VP3 gene en-subtitle= kn-subtitle= en-abstract= kn-abstract=Group C rotavirus (GCRV) is distributed worldwide as an enteric pathogen in humans and animals. However, to date, whole-genome sequences are available only for a human strain (Bristol) and a porcine strain (Cowden). To investigate the genetic diversity of human GCRVs, nearly full-length sequences of all 11 RNA segments were determined for human GCRVs detected recently in India (v508), Bangladesh (BS347), China (Wu82 and YNR001) and Japan (OH567 and BK0830) and analysed phylogenetically with sequence data for GCRVs published previously. All the RNA segments of human GCRV strains except for the VP3 gene showed high levels of conservation (>93?% nucleotide sequence identity, >92?% amino acid sequence identity), belonging to a single genetic cluster distinct from those of animal GCRVs. In contrast, the VP3 genes of human GCRVs could be discriminated into two clusters, designated M2 and M3, that were distinguished phylogenetically from those of porcine and bovine GCRVs (clusters M1 and M4, respectively). Between M2 and M3, amino acid sequence identity of the VP3 gene was 84.1?84.7?%, whereas high identities were observed within each cluster (92.3?97.6?% for M2, 98.2?99.3?% for M3). Sequence divergence among the four VP3 clusters was observed throughout the amino acid sequence except for conserved motifs, including those possibly related to enzyme functions of VP3. The presence of obvious genetic diversity only in the VP3 gene among human GCRVs suggested that either the M2 or M3 VP3 gene of human GCRVs might have been derived through reassortment from an animal GCRV or from an unidentified human GCRV strain belonging to a novel genogroup. en-copyright= kn-copyright= en-aut-name=YamamotoDai en-aut-sei=Yamamoto en-aut-mei=Dai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=GhoshSouvik en-aut-sei=Ghosh en-aut-mei=Souvik kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KuzuyaMitsutaka en-aut-sei=Kuzuya en-aut-mei=Mitsutaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WangYuan-Hong en-aut-sei=Wang en-aut-mei=Yuan-Hong kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ZhouXuan en-aut-sei=Zhou en-aut-mei=Xuan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Chawla-SarkarMamta en-aut-sei=Chawla-Sarkar en-aut-mei=Mamta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=PaulShyamal Kumar en-aut-sei=Paul en-aut-mei=Shyamal Kumar kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IshinoMasaho en-aut-sei=Ishino en-aut-mei=Masaho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KobayashiNobumichi en-aut-sei=Kobayashi en-aut-mei=Nobumichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=2 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=3 en-affil= kn-affil=Okayama Prefectural Institute for Environmental Science and Public Health affil-num=4 en-affil= kn-affil=Wuhan Centers for Disease Prevention and Control affil-num=5 en-affil= kn-affil=Wuhan Centers for Disease Prevention and Control affil-num=6 en-affil= kn-affil=National Institute of Cholera and Enteric Diseases affil-num=7 en-affil= kn-affil=Mymensingh Medical College affil-num=8 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=9 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine END start-ver=1.4 cd-journal=joma no-vol=91 cd-vols= no-issue=9 article-no= start-page=2367 end-page=2373 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201009 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Complete genome constellation of a caprine group A rotavirus strain reveals common evolution with ruminant and human rotavirus strains en-subtitle= kn-subtitle= en-abstract= kn-abstract=This study reports the first complete genome sequence of a caprine group A rotavirus (GAR) strain, GO34. The VP7-VP4-VP6-VP1-VP2-VP3-NSP1-NSP2-NSP3-NSP4-NSP5 genes of strain GO34, detected in Bangladesh, were assigned to the G6-P[1]-I2-R2-C2-M2-A11-N2-T6-E2-H3 genotypes, respectively. Strain GO34 was closely related to the VP4, VP6?7 and NSP4?5 genes of bovine GARs and the NSP1 gene of GO34 to an ovine GAR. Strain GO34 shared low nucleotide sequence identities (<90?%) with VP2?3 genes of other GARs, and was equally related to NSP3 genes of human, ruminant and camelid strains. The VP1, VP6 and NSP2 genes of strain GO34 also exhibited a close genetic relatedness to human G2, G6, G8 and G12 DS-1-like GARs, whereas the NSP1 of GO34 was also closely related to human G6P[14] strains. All these findings point to a common evolutionary origin of GO34 and bovine, ovine, antelope, guanaco and human G6P[14] GARs, although phylogenetically GO34 is not particularly closely related to any other rotavirus strains known to date. en-copyright= kn-copyright= en-aut-name=GhoshSouvik en-aut-sei=Ghosh en-aut-mei=Souvik kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AlamMohammed Mahbub en-aut-sei=Alam en-aut-mei=Mohammed Mahbub kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AhmedMuzahed Uddin en-aut-sei=Ahmed en-aut-mei=Muzahed Uddin kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TalukdarRafiqul Islam en-aut-sei=Talukdar en-aut-mei=Rafiqul Islam kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=PaulShyamal Kumar en-aut-sei=Paul en-aut-mei=Shyamal Kumar kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KobayashiNobumichi en-aut-sei=Kobayashi en-aut-mei=Nobumichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=2 en-affil= kn-affil=Department of Medicine, Faculty of Veterinary Science, Bangladesh Agricultural University affil-num=3 en-affil= kn-affil=Department of Medicine, Faculty of Veterinary Science, Bangladesh Agricultural University affil-num=4 en-affil= kn-affil=Department of Medicine, Faculty of Veterinary Science, Bangladesh Agricultural University affil-num=5 en-affil= kn-affil=Department of Microbiology, Mymensingh Medical College affil-num=6 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine END start-ver=1.4 cd-journal=joma no-vol=91 cd-vols= no-issue=7 article-no= start-page=1772 end-page=1781 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201007 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Analysis of genetic diversity and molecular evolution of human group B rotaviruses based on whole genome segments en-subtitle= kn-subtitle= en-abstract= kn-abstract=Group B rotavirus (GBR) is a rare enteric pathogen that causes severe diarrhoea, primarily in adults. Nearly full-length sequences of all 11 RNA segments were determined for human GBRs detected recently in India (IDH-084 in 2007, IC-008 in 2008), Bangladesh (Bang117 in 2003) and Myanmar (MMR-B1 in 2007), and analysed phylogenetically with the sequence data of GBRs reported previously. All RNA segments of GBR strains from India, Bangladesh and Myanmar showed >95?% nucleotide sequence identities. Among the 11 RNA segments, the VP6 and NSP2 genes showed the highest identities (>98?%), whilst the lowest identities were observed in the NSP4 gene (96.1?%), NSP5 gene (95.6?%) and VP8*-encoding region of the VP4 gene (95.9?%). Divergent or conserved regions in the deduced amino acid sequences of GBR VP1?VP4 and NSP1?NSP5 were similar to those in group A rotaviruses (GARs), and the functionally important motifs and structural characteristics in viral proteins known for GAR were conserved in all of the human GBRs. These findings suggest that, whilst the degree of genetic evolution may be dependent on each RNA segment, human GBR may have been evolving in a similar manner to GAR, associated with the similar functional roles of individual viral proteins. en-copyright= kn-copyright= en-aut-name=YamamotoDai en-aut-sei=Yamamoto en-aut-mei=Dai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=GhoshSouvik en-aut-sei=Ghosh en-aut-mei=Souvik kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=GaneshBalasubramanian en-aut-sei=Ganesh en-aut-mei=Balasubramanian kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KrishnanTriveni en-aut-sei=Krishnan en-aut-mei=Triveni kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=Chawla-SarkarMamta en-aut-sei=Chawla-Sarkar en-aut-mei=Mamta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AlamMohammed Mahbub en-aut-sei=Alam en-aut-mei=Mohammed Mahbub kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=AungTin Sabai en-aut-sei=Aung en-aut-mei=Tin Sabai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KobayashiNobumichi en-aut-sei=Kobayashi en-aut-mei=Nobumichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=2 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine affil-num=3 en-affil= kn-affil=National Institute of Cholera and Enteric Diseases affil-num=4 en-affil= kn-affil=National Institute of Cholera and Enteric Diseases affil-num=5 en-affil= kn-affil=National Institute of Cholera and Enteric Diseases affil-num=6 en-affil= kn-affil=Bangladesh Agricultural University affil-num=7 en-affil= kn-affil=National Health Laboratory affil-num=8 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine END start-ver=1.4 cd-journal=joma no-vol=155 cd-vols= no-issue=2 article-no= start-page=159 end-page=167 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20091121 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Molecular characterization of the VP1, VP2, VP4, VP6, NSP1 and NSP2 genes of bovine group B rotaviruses: identification of a novel VP4 genotype en-subtitle= kn-subtitle= en-abstract= kn-abstract=Studies on bovine group B rotaviruses (GBRs) are limited. To date, only the VP6 gene of a single bovine GBR strain and the VP7 and NSP5 genes of a few bovine GBR strains have been sequenced and analyzed. In the present study, using a single-primer amplification method, we have determined the full-length nucleotide sequences of the VP1, VP2, VP4, VP6, NSP1 and NSP2 genes of three bovine GBR strains from eastern India. In all six of these genes, the bovine GBR strains shared high genetic relatedness among themselves but exhibited high genetic diversity with cognate genes of human, murine and ovine GBRs. Interestingly, as with group A rotaviruses, the bovine GBR VP1, VP2, VP6 and NSP2 genes appeared to be more conserved than the VP4 and NSP1 genes among strains of different species. The present study provides important insights into the genetic makeup and diversity of bovine GBRs, and also identifies a novel GBR VP4 genotype. en-copyright= kn-copyright= en-aut-name=GhoshS en-aut-sei=Ghosh en-aut-mei=S kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KobayashiN en-aut-sei=Kobayashi en-aut-mei=N kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NagashimaS en-aut-sei=Nagashima en-aut-mei=S kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Chawla-SarkarM en-aut-sei=Chawla-Sarkar en-aut-mei=M kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KrishnanT en-aut-sei=Krishnan en-aut-mei=T kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=GaneshB en-aut-sei=Ganesh en-aut-mei=B kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NaikTN en-aut-sei=Naik en-aut-mei=TN kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine, S 1,W 17, Chuo-Ku, Sapporo affil-num=2 en-affil= kn-affil=Department of Hygiene, Sapporo Medical University School of Medicine, S 1,W 17, Chuo-Ku, Sapporo affil-num=3 en-affil= kn-affil=Division of Virology, Department of Infection and Immunity, Jichi Medical University School of Medicine affil-num=4 en-affil= kn-affil=Division of Virology, National Institute of Cholera and Enteric Diseases affil-num=5 en-affil= kn-affil=Division of Virology, National Institute of Cholera and Enteric Diseases affil-num=6 en-affil= kn-affil=Division of Virology, National Institute of Cholera and Enteric Diseases affil-num=7 en-affil= kn-affil=School of Biology, National Institute of Science Education and Research END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=1 article-no= start-page=83 end-page=85 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Complications of hand-foot-mouth disease kn-title=手足口病の合併症 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name=山下信子 kn-aut-sei=山下 kn-aut-mei=信子 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　病原ウイルス学 END start-ver=1.4 cd-journal=joma no-vol=409 cd-vols= no-issue=4 article-no= start-page=663 end-page=668 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110617 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Plural assay systems derived from different cell lines and hepatitis C virus strains are required for the objective evaluation of anti-hepatitis C virus reagents en-subtitle= kn-subtitle= en-abstract= kn-abstract=Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. HuH-7 hepatoma-derived cells are widely used as the only cell-based HCV replication system for HCV research, including drug assays. Recently, using different hepatoma Li23-derived cells, we developed an HCV drug assay system (ORL8), in which the genome-length HCV RNA (O strain of genotype 1b) encoding renilla luciferase replicates efficiently. In this study, using the HuH-7-derived OR6 assay system that we developed previously and the ORL8 assay system, we evaluated 26 anti-HCV reagents, which other groups had reported as anti-HCV candidates using HuH-7-derived assay systems other than ORB. The results revealed that more than half of the reagents showed different anti-HCV activities from those in the previous studies, and that anti-HCV activities evaluated by the ORB and ORL8 assays were also frequently different. In further evaluation using the HuH-7-derived AH1R assay system, which was developed using the AH1 strain of genotype 1b, several reagents showed different anti-HCV activities in comparison with those evaluated by the OR6 and ORL8 assays. These results suggest that the different activities of anti-HCV reagents are caused by the differences in cell lines or HCV strains used for the development of assay systems. Therefore, we conclude that plural HCV assay systems developed using different cell lines or HCV strains are required for the objective evaluation of anti-HCV reagents. en-copyright= kn-copyright= en-aut-name=UedaYouki en-aut-sei=Ueda en-aut-mei=Youki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MoriKyoko en-aut-sei=Mori en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences en-keyword=HCV kn-keyword=HCV en-keyword=HCV RNA replication system kn-keyword=HCV RNA replication system en-keyword=Li23 cells kn-keyword=Li23 cells en-keyword=Reporter assay for anti-HCV reagents kn-keyword=Reporter assay for anti-HCV reagents END start-ver=1.4 cd-journal=joma no-vol=123 cd-vols= no-issue=1 article-no= start-page=27 end-page=31 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Renato Dulbecco: Dulbecco’s modified Eagle’s medium kn-title=Renato Dulbecco ： ダルベッコ培地 en-subtitle= kn-subtitle= en-abstract= kn-abstract=現在，医学分野の多くの研究は培養細胞や培養組織を用いてなされている．それらの研究成果が報告されている論文の“材料と方法”の項で，ダルベッコ培地を使用して細胞を培養したといった記載を読んだ研究者は少なくないであろう．また，実際にダルベッコ培地を使用した研究者もいると思う．今回は，この培地を報告したDulbecco（1975年，がんウイルスの研究によってノーベル賞）の波乱万丈の経歴，彼の人脈（多くの人物がノーベル賞を受賞），彼の研究概略などについて紹介したい．そして，筆者のダルベッコ培地に対する見解とその培地を使用した経験について述べる．筆者の結論は，初代細胞培養にはダルベッコ培地が勧められること，また，培養細胞を用いての毒性検定に際しては，使用する培地によって結果が異なることがあるので注意する必要があることである． en-copyright= kn-copyright= en-aut-name=NambaMasayoshi en-aut-sei=Namba en-aut-mei=Masayoshi kn-aut-name=難波正義 kn-aut-sei=難波 kn-aut-mei=正義 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=新見公立大学，岡山医学振興会 en-keyword=Renato Dulbecco kn-keyword=Renato Dulbecco en-keyword=ダルベッコ培地 kn-keyword=ダルベッコ培地 en-keyword=ノーベル賞 kn-keyword=ノーベル賞 en-keyword=Dulbeccoの人脈 kn-keyword=Dulbeccoの人脈 END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=9-2 article-no= start-page=5929 end-page=5945 dt-received= dt-revised= dt-accepted= dt-pub-year=1959 dt-pub=19590910 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the Pathogene of Infectious Hepatitis Part I Experimental Studies by the Newly Isolated Virus from Hepatitis Patient kn-title=流行性肝炎の病原体に関する研究 第1編 肝炎患者より新に分離したウイルスを用いて行つた実験的研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=MURAKAMI and his collaborator had isolated the hepatitis virus from hepatitis patient and cultured in the chorio-allantoic cavity of chick embryo. The author newly isolated the hepatitis virus from the patient and studied on virological properties of the virus having obtained the purified virus. The following results were obtained. 1) In the treatment by heating or by disinfectant, the purified virus showed high resistance to these treatment, and these resistances were thought to be the featuring properties of the virus. 2) Also it was observed that the virus was highly resistant to irradiation of ultraviolet rays, and to action of ether. 3) The purified virus was highly infections to mouse by peroral administration of it. The pathological changes were observed conspicuously, and moreover the changes induced were just the identical in any case. 4) By the serological study, it was observed that the purified virus had an eminent antigenic capacity and reacted with the immune serum obtained by inoculation of the virus to rabbit giving the antigenic titier of 1:64-1:128. Also the virus showed distinctive reaction in the complement fixation test using the convalescent patient's serum from hepatitis; hence, this test might be highly valuable for the serological diagnosis of hepatitis despite of rather low titer than the above. 5) The most difficult problem was the identification of neutralizing effect in the neutralization test and “Abs?ttigungsversuch”. For this purpose the author adopted the mitigation of pathological changes caused by the neutralizing effect and observed the marked mitigation of the changes on the test using the virus and corrsponding immune serum; but this evidence was not observed in the test of the virus and uncorresponding serum. The mitigation of the changes was not distinct in the "Abs?ttigungsversuch" possibly by the occurence of combination of the virus and its anti-body in the body of animal instead of in the test tube. It is to be expected the further study on the test procedure and the method of identifying the neutralization effect. en-copyright= kn-copyright= en-aut-name=SengokuAkihisa en-aut-sei=Sengoku en-aut-mei=Akihisa kn-aut-name=仙石晃久 kn-aut-sei=仙石 kn-aut-mei=晃久 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部微生物学教室 END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=9-2 article-no= start-page=5827 end-page=5835 dt-received= dt-revised= dt-accepted= dt-pub-year=1959 dt-pub=19590910 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the Purified Heratitis Virus Part I Comparative Studies on Virological Properties with IZUMI Fever Virus kn-title=精製肝炎ウイルスに関する研究 第1編 精製ウイルスの比較研究殊に泉熱ウイルスとの比較 en-subtitle= kn-subtitle= en-abstract= kn-abstract=MURAKAMI and his collaborator had reported already the properties of the hepatitis virus isolated from hepatitis patient in detail, and they pointed out some similarity of the virus with the IZUMI fever virus. The author obtained both viruses in purified form by means of ultracentrifuge, and carried out further investigation on the virological properties of these viruses. The following results were obtained. 1) It was confirmed that both viruses could be obtainable easily and efficiently in purified form by means of ultracentrifuge, and showed powerful pathogenecity to mouse capable of inducing the typical pathological changes by infection; however, the infection of either virus did not render the lethal effect and was detectable as latent infection in that only the pathological findings were informative. And by the electronmicroscopical study, both viruses were observed in minute round or oval form whose diameter was 50-70 mμ. 2) From the viewpoint of the virological properties, both viruses were much different in the resistance to heat and disinfectant: the purified hepatitis virus could stand aginst heating at 70°-75°C and against the action of disinfectant, 0.2% formalin or 0.01% marzonin, for less than 3 weeks; on the other hand the IZUMI fever virus was inactivated by heating 55°-60°C for 30 min. or by action of the disinfectant for 2 weeks. 3) By the irradiation of ultraviolet rays, it is needed to inactivate the purified hepatitis virus for 40 min. irradiation, but in the case of IZUMI fever virus it was completely inactivated by only 5-20 min. irradiation. en-copyright= kn-copyright= en-aut-name=TsudaTetsuro en-aut-sei=Tsuda en-aut-mei=Tetsuro kn-aut-name=津田哲郎 kn-aut-sei=津田 kn-aut-mei=哲郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部微生物学教室 END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=1 article-no= start-page=1 end-page=9 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201002 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Epidemiology of Chlamydophila caviae-like Chlamydia Isolated from Urethra and Uterine Cervix en-subtitle= kn-subtitle= en-abstract= kn-abstract=

In 2000, chlamydial strains OK133 and OK135 were isolated from 2 female patients with cervicitis. These strains were unresponsive to commercially available PCR and LCR test kits for the diagnosis of Chlamydia trachomatis infection, and their phenotypic characteristics were very similar. The OK135 nucleotide sequence in MOMP-VD2 gene closely resembled that of Chlamydophila caviae GPIC. A similar strain was isolated in 2003 from a male patient OKM2 with urethritis, from which the strain SC10-6 was cloned by the plaque purification method. The nucleotide sequence of the entire MOMP gene of SC10-6 was exactly the same as that of OK135. Thus, the strains OK135 and SC10-6, together with OK133, have been called C. caviae-like Chlamydia. We designed primers for nested PCR assay, the product of which showed a single-band 311-bp fragment, to detect C. caviae-like Chlamydia. Of swab specimens obtained from 202 patients from 2003 to 2006 (119 male and 83 female patients), 18 specimens (8.9%) from 14 male and 4 female patients were positive, suggesting that C. caviae-like Chlamydia infection is rather common. Thus far, it has not been determined whether C. caviae-like Chlamydia is pathogenic for humans.

en-copyright= kn-copyright= en-aut-name=MuraoWataru en-aut-sei=Murao en-aut-mei=Wataru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=WadaKoichiro en-aut-sei=Wada en-aut-mei=Koichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsumotoAkira en-aut-sei=Matsumoto en-aut-mei=Akira kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FujiwaraMichihisa en-aut-sei=Fujiwara en-aut-mei=Michihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FukushiHideto en-aut-sei=Fukushi en-aut-mei=Hideto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KishimotoToshio en-aut-sei=Kishimoto en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MondenKoichi en-aut-sei=Monden en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KariyamaReiko en-aut-sei=Kariyama en-aut-mei=Reiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KumonHiromi en-aut-sei=Kumon en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Obstetrics and Gynecology, Kawasaki Hospital affiliated with Kawasaki Medical School affil-num=5 en-affil= kn-affil=Department of Applied Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University affil-num=6 en-affil= kn-affil=Department of Virology I, The National Institute of Infectious Diseases affil-num=7 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=Chlamydophila caviae-like Chlamydia kn-keyword=Chlamydophila caviae-like Chlamydia en-keyword=urethra kn-keyword=urethra en-keyword=uterine cervix kn-keyword=uterine cervix en-keyword=epidemiology kn-keyword=epidemiology en-keyword=sexually transmitted infection kn-keyword=sexually transmitted infection END start-ver=1.4 cd-journal=joma no-vol=28 cd-vols= no-issue=4 article-no= start-page=247 end-page=252 dt-received= dt-revised= dt-accepted= dt-pub-year=1974 dt-pub=197408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Attempts to isolate virus from human brain tumors en-subtitle= kn-subtitle= en-abstract= kn-abstract=

In order to study the viral etiology of human brain tumors, attempts were made to isolate cytopathogenic agents from human brain tumors by the tissue culture of tumor tissues and by the mixed culture of tumor tissues with HeLa cells. Five glioblastomas, a mixed form of glioblastoma and fibrosarcoma, two astrocytomas, two ependymomas, two meningiomas, an oligodendroglioma, a spongioblastoma polare and a choroid plexus papilloma were studied. In the tissue culture, besides the cells which appeared to be the tumor parenchymal cells, varying amounts of fibroblastic cells appeared in all the tumors tested and they increased with the prolongation of the culture period. In any of the tumors tested, no cytopathogenic agents were detected by either the culture of tumor tissues or the mixed culture of tumor tissues with HeLa cells. From the virological point of view, the significance of these negative results was discussed.

en-copyright= kn-copyright= en-aut-name=YabeYoshiro en-aut-sei=Yabe en-aut-mei=Yoshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University END start-ver=1.4 cd-journal=joma no-vol=45 cd-vols= no-issue=1 article-no= start-page=43 end-page=47 dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=199102 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Reactivatable latency of three avirulent strains of herpes simplex virus type 1 after intranasal inoculation in mice. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

In order to elucidate the mechanism of latent infection of herpes simplex virus (HSV), reactivatable latency of three avirulent strains (SKO-1B, -GCr Miyama, SKa) of HSV type 1 was comparatively examined in a mouse latency model. The SKO-1B strain showed high rate of virus reactivation from explanted trigeminal ganglia without n-butyrate enhancement, while the other two strains showed a very low rate of virus reactivation in the absence of n-butyrate. In the presence of n-butyrate, however, the rate of the -GCr Miyama strain jumped to a comparable level with that of SKO-1B, although the rate of SKa remained at a low level. A more precise follow-up experiment changing the virus dose highlighted the difference of the ability to reactivate from the latent state between SKO-1B and -GCr Miyama. Virus titer in trigeminal ganglia during acute phase, infectivity to cell lines of neural origin, and susceptibility to acyclovir and phosphonoacetate were assayed to know the reasons for the variation in the ability of reactivatable latency among these strains. It was concluded that the reduced infectivity to neural cells, and limited ability of reactivatable latency shown by the SKa strain could mainly be attributed to the deficiency of thymidine kinase activity.</P>

en-copyright= kn-copyright= en-aut-name=AraoYujiro en-aut-sei=Arao en-aut-mei=Yujiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HatanoAtsushi en-aut-sei=Hatano en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=UnoFumio en-aut-sei=Uno en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NiiShiro en-aut-sei=Nii en-aut-mei=Shiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=The University of Tokushima affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Niimi Women's College affil-num=5 en-affil= kn-affil=Okayama University en-keyword=herpes simplex virus type 1 kn-keyword=herpes simplex virus type 1 en-keyword=neurovirulence kn-keyword=neurovirulence en-keyword=latency kn-keyword=latency en-keyword=reactivation kn-keyword=reactivation en-keyword=n-butyrate kn-keyword=n-butyrate END start-ver=1.4 cd-journal=joma no-vol=45 cd-vols= no-issue=2 article-no= start-page=117 end-page=121 dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=199104 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Neurovirulent strains of herpes simplex virus type 1 are not necessarily competent for reactivatable latency. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Ability of two neurovirulent strains (F and +GC (LPV) Miyama) of herpes simplex virus type 1 (HSV-1) to establish and maintain reactivatable latency in trigeminal ganglia (TG) was compared after intranasal inoculation of mice. The +GC (LPV) Miyama strain showed a very low rate of virus reactivation in explant cultures of TG, while the F strain showed a high rate of reactivation. These data indicate that neurovirulent strains of HSV-1 are not always competent for reactivatable latency, although most virulent strains of HSV-1 thus far reported were competent for reactivatable latency.</P>

en-copyright= kn-copyright= en-aut-name=AraoYujiro en-aut-sei=Arao en-aut-mei=Yujiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HatanoAtsushi en-aut-sei=Hatano en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=UnoFumio en-aut-sei=Uno en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NiiShiro en-aut-sei=Nii en-aut-mei=Shiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=The University of Tokushima affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Niimi Woman's College affil-num=5 en-affil= kn-affil=Okayama University en-keyword=herpes simplex virus type 1 kn-keyword=herpes simplex virus type 1 en-keyword=neurovirulence kn-keyword=neurovirulence en-keyword=latency kn-keyword=latency en-keyword=reactivation kn-keyword=reactivation END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=2 article-no= start-page=67 end-page=74 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Induction and prevention of virus-associated malignant lymphoma by serial transmission of EBV-related virus from cynomolgus by blood transfusion in rabbits. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Epstein-Barr virus (EBV)-related herpesvirus (Si-IIA-EBV) was serially transmitted for 3 passages from rabbit to rabbit of the opposite sex by blood transfusion, which subsequently induced virus-associated rabbit lymphomas. The virus could be transmitted by transfusion with 15-20 ml of whole blood (7/7) or irradiated blood (1/6) from the EBV-related virus-infected rabbits, but there was no transmission with transfusion of cell-free plasma (0/6) from the infected rabbits. Passive anti-EBV-VCA IgG (x 20 approximately x 10) titers decreased during the first 1-2 weeks in the transfused rabbits. The virus-transmitted rabbits showed a gradual increase in antibody titers ranging from peak titers of x 640 to x 2560 after 3 weeks of transfusion. The recipient origin of malignant lymphoma that developed in the first rabbit transfused by infected blood was confirmed by chromosomal analysis. This rabbit model thus shows that EBV-related herpesvirus is serially transmissible by blood transfusion and that transmission can not be completely prevented by irradiation of blood, but removal of blood cells is the best way to prevent transmission of EBV-related virus. Therefore, this animal model provides a convenient in vivo system for studies of the prevention and therapy of transfusion-related transmission of EBV and EBV-associated lymphoproliferative diseases in immunocompromised human beings.

en-copyright= kn-copyright= en-aut-name=KoiralaTirtha Raj en-aut-sei=Koirala en-aut-mei=Tirtha Raj kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=JinZaishun en-aut-sei=Jin en-aut-mei=Zaishun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OnodaSachiyo en-aut-sei=Onoda en-aut-mei=Sachiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OdaWakako en-aut-sei=Oda en-aut-mei=Wakako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IchimuraKoichi en-aut-sei=Ichimura en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OharaNobuya en-aut-sei=Ohara en-aut-mei=Nobuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YamadaMasao en-aut-sei=Yamada en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Tottori University, Tottori affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University affil-num=11 en-affil=Okayama University kn-affil= en-keyword=?Epstein-Barr virus(EBV) kn-keyword=?Epstein-Barr virus(EBV) en-keyword=rabbit kn-keyword=rabbit en-keyword=lymphoproliferative diseases kn-keyword=lymphoproliferative diseases en-keyword=blood transfusion kn-keyword=blood transfusion END start-ver=1.4 cd-journal=joma no-vol=55 cd-vols= no-issue=3 article-no= start-page=133 end-page=159 dt-received= dt-revised= dt-accepted= dt-pub-year=2001 dt-pub=200106 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Molecular virology of hepatitis C virus. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Hepatitis C virus (HCV), discovered in 1989, is the major causative agent of parenteral non-A, non-B hepatitis worldwide. Following the development of a method of diagnosing HCV infection, it became apparent that HCV frequently causes chronic hepatitis. Persistent infection with HCV is implicated in liver cirrhosis and hepatocellular carcinoma. Current worldwide estimations suggest that more than 170 million people have been infected with HCV, an enveloped positive single-stranded RNA (9.6-kilobases) virus belonging to the Flaviviridae. The HCV genome shows remarkable sequence variation, especially in the hypervariable region 1 of the E2 protein-encoding region, and globally, HCV appears to be distributed with more than 30 genotypes. Complicated "quasispecies" and frequent mutations of viral genomes have also emerged. The HCV genome encodes a large polyprotein precursor of about 3,000 amino acid residues, and this precursor protein is cleaved by the host and viral proteinases to generate at least 10 proteins in the following order: NH2-core-envelope (E1)-E2-p7-nonstructural protein 2 (NS2)-NS3-NS4A-NS4B-NS5A-NS5B-COOH. These viral proteins not only function in viral replication but also affect a variety of cellular functions. Although several explanations have been proposed, the mechanisms of HCV infection and replication in targeted cells, the mechanism of persistent viral infection, and the pathogenesis of hepatic diseases (hepatitis or hepatocellular carcinoma) are all poorly understood. A major reason why these mechanisms remain unclear is the lack of a good experimental HCV replication system. Although several classical trials using cultured cells have been reported, several new, more promising experimental strategies (generations of infectious cDNA clone, replicon, animal models, etc.) are currently being designed and tested, in order to resolve these problems. In addition, new therapies for chronic hepatitis have also been developed. The enormous body of information collected thus far in the field of HCV research is summarized below, and an overview of the current status of HCV molecular virology of HCV is provided.</P>

en-copyright= kn-copyright= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University END start-ver=1.4 cd-journal=joma no-vol=59 cd-vols= no-issue=6 article-no= start-page=239 end-page=246 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=200512 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Virological aspects of Epstein-Barr virus infections. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Epstein-Barr virus (EBV) is usually maintained in an asymptomatic and latent form by the host immune system, and primarily by EBV-specific cytotoxic T cells (CTLs). However, EBV has been linked to several refractory diseases such as EBV-associated hemophagocytic syndrome(EBV-AHS) and chronic active EBV infection (CAEBV). In these ectopic diseases, EBV infects T/NK cells, causing severe immunodeficiency with a very high EBV load. In recent years, the laboratory procedure to assess these types of EBV infections has been improved. In particular, real-time polymerase chain reaction (PCR) has been used to quantify the EBV load, and the MHC: peptide tetramer assay has been used to quantitate EBV-specific CTLs; these tests have been employed for the management of the illnesses associated with EBV infection. Here, we have reviewed the recent progress in the clinical application of these assays. The pathogenesis of EBV-infected T/NK cells, and the host immune response to infection, including the roles carried out by innate immunity and inflammatory cytokines, are likely to be revealed in the future.

en-copyright= kn-copyright= en-aut-name=YamashitaNobuko en-aut-sei=Yamashita en-aut-mei=Nobuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KimuraHiroshi en-aut-sei=Kimura en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MorishimaTsuneo en-aut-sei=Morishima en-aut-mei=Tsuneo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Nagoya University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=chronic active Epstein-Barr virus infection kn-keyword=chronic active Epstein-Barr virus infection en-keyword=Epstein-Barr virus-associated hemophagocytic syndrome kn-keyword=Epstein-Barr virus-associated hemophagocytic syndrome en-keyword=Real-time PCR kn-keyword=Real-time PCR en-keyword=tetramer kn-keyword=tetramer END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue=4 article-no= start-page=327 end-page=337 dt-received= dt-revised= dt-accepted= dt-pub-year=1957 dt-pub=195712 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Some observations on the outbreak of encepalo-meningornyelitis encountered in Ehime Syuso area through tweenty-eight hospitalized patients (1956) en-subtitle= kn-subtitle= en-abstract= kn-abstract=

An outbreak of encephalomeningomyelitis in Ehime?Syuso area from April to June 1956 was clinico-virologically investigated with the materials obtained from 28 hospitalized cases and their healthy visiting relatives. The major rise in polio type I antibody titer and the positive isolation of 4 strains of type I indicate the epidemy in this area to be the polio type 1. Three undeterminable cytopathogenic agents were concomitantly obtained in the HeLa cultures. The style of this episode was duly compared with the documents already reported.

en-copyright= kn-copyright= en-aut-name=KitamuraIsamu en-aut-sei=Kitamura en-aut-mei=Isamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University END start-ver=1.4 cd-journal=joma no-vol=25 cd-vols= no-issue=6 article-no= start-page=643 end-page=648 dt-received= dt-revised= dt-accepted= dt-pub-year=1971 dt-pub=197112 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Electron microscopic, immunofluorescent and virological studies on a rhabdomyosarcoma in epidermodysplasia verruciformis en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A subcutaneous tumor of a patient with epidermodysplasia verruciformis was studied by the light microscopy, the electronmicroscopy and the immunofluorescent test. The tumor cells were histologically pleomorphic and electronmicroscopically contained varying amounts of cytoplasmic filaments without Z-band formation. The antimyosin serum stained the tumor cells, showing their myogenic origin. No virus or virus-like particles were observed in the tumor. Tumor antigens stainable by the patient's serum were not detected. Hamsters inoculated with the tumor extract at birth developed no noticeable diseases.

en-copyright= kn-copyright= en-aut-name=YabeYoshiro en-aut-sei=Yabe en-aut-mei=Yoshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KoyamaHiroko en-aut-sei=Koyama en-aut-mei=Hiroko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University END start-ver=1.4 cd-journal=joma no-vol=49 cd-vols= no-issue=3 article-no= start-page=137 end-page=144 dt-received= dt-revised= dt-accepted= dt-pub-year=1995 dt-pub=199506 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Virological and serological characterization of asymptomatic blood donors positive for anti-hepatitis C virus antibody. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To study the virological and serological characteristics of asymptomatic hepatitis C virus (HCV) carriers, 165 blood donors positive for antibody against HCV proteins by the second generation assay, were analyzed for their clinical backgrounds, serological reactivity against antigens derived from HCV by recombinant immunoblot assay, and the amount and genotype of HCV by the polymerase chain reaction. Compared with blood donors having abnormal levels of alanine aminotransferase (ALT), sera from the donors with normal levels of ALT reacted less frequently against NS4 antigens (anti-5-1-1: 34.4% vs. 54.5%, P = 0.0609; anti-c100-3: 34.4% vs. 56.1%, P < 0.05). Also the positivity for antibodies against these antigens were more frequent in sera from donors with genotype 1b HCV-RNA than other genotypes (anti-5-1-1: 61.0% vs. 23.5%, P < 0.01; anti-c 100-3: 61.0% vs. 26.5%, P < 0.01). The prevalence of each genotype in blood donors with normal ALT levels was different from that in patients with advanced liver disease (P < 0.05), genotype 1b being less and genotype 2a being more frequent. The number of HCV-RNA copies/0.5 ml in donors with normal ALT was 10(7.9 +/- 1.0) (n = 27) and that in patients with chronic liver disease was 10(7.4 +/- 0.8) (n = 116), the difference being statistically significant (P < 0.05). In conclusion, the results of this study suggest that asymptomatic blood donors carrying HCV have the serological and virological characteristics different from the patients with advanced liver disease.

en-copyright= kn-copyright= en-aut-name=TsujiHideyuki en-aut-sei=Tsuji en-aut-mei=Hideyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ShimomuraHiroyuki en-aut-sei=Shimomura en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=WatoMasaki en-aut-sei=Wato en-aut-mei=Masaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KondoJunichi en-aut-sei=Kondo en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TsujiTakao en-aut-sei=Tsuji en-aut-mei=Takao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=hepatitis C virus kn-keyword=hepatitis C virus en-keyword=blood donor kn-keyword=blood donor en-keyword=asymptomatic carrier kn-keyword=asymptomatic carrier END start-ver=1.4 cd-journal=joma no-vol=122 cd-vols= no-issue=1 article-no= start-page=33 end-page=38 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20100401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Contribution of cell cultures to the Nobel Prize kn-title=細胞培養のノーベル賞への貢献 en-subtitle= kn-subtitle= en-abstract= kn-abstract=約1世紀前に, 生きた組織や細胞を動物の体外に取り出した研究―組織培養あるいは細胞培養―が始まった．その後の研究の流れの中で, 1) 組織・細胞培養の特性を生かして行われた研究でノーベル賞に輝いた研究, 2) 組織・細胞培養の経験をもつノーベル賞受賞者, 3) ノーベル賞にはならなかったけれども特記できると私が考える細胞培養の研究，などについて取り上げてみたい. en-copyright= kn-copyright= en-aut-name=NambaMasayoshi en-aut-sei=Namba en-aut-mei=Masayoshi kn-aut-name=難波正義 kn-aut-sei=難波 kn-aut-mei=正義 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=新見公立大学 en-keyword=細胞 kn-keyword=細胞 en-keyword=培養 kn-keyword=培養 en-keyword=ノーベル賞 kn-keyword=ノーベル賞 END start-ver=1.4 cd-journal=joma no-vol=122 cd-vols= no-issue=1 article-no= start-page=9 end-page=16 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20100401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The DNA damage sensors ataxia-telangiectasia mutated kinase and checkpoint kinase 2 are required for hepatitis C virus RNA replication kn-title=DNA 損傷センサーATMキナーゼとChk2はＣ型肝炎ウイルスのRNA複製に必要である en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=AriumiYasuo en-aut-sei=Ariumi en-aut-mei=Yasuo kn-aut-name=有海康雄 kn-aut-sei=有海 kn-aut-mei=康雄 aut-affil-num=1 ORCID= en-aut-name=KurokiMisao en-aut-sei=Kuroki en-aut-mei=Misao kn-aut-name=黒木美沙緒 kn-aut-sei=黒木 kn-aut-mei=美沙緒 aut-affil-num=2 ORCID= en-aut-name=DansakoHiromichi en-aut-sei=Dansako en-aut-mei=Hiromichi kn-aut-name=團迫浩方 kn-aut-sei=團迫 kn-aut-mei=浩方 aut-affil-num=3 ORCID= en-aut-name=AbeKenichi en-aut-sei=Abe en-aut-mei=Kenichi kn-aut-name=阿部健一 kn-aut-sei=阿部 kn-aut-mei=健一 aut-affil-num=4 ORCID= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name=池田正徳 kn-aut-sei=池田 kn-aut-mei=正徳 aut-affil-num=5 ORCID= en-aut-name=WakitaTakaji en-aut-sei=Wakita en-aut-mei=Takaji kn-aut-name=脇田隆字 kn-aut-sei=脇田 kn-aut-mei=隆字 aut-affil-num=6 ORCID= en-aut-name=KatoNobuyuki en-aut-sei=Kato en-aut-mei=Nobuyuki kn-aut-name=加藤宣之 kn-aut-sei=加藤 kn-aut-mei=宣之 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 affil-num=6 en-affil= kn-affil=国立感染症研究所　ウイルス第二部 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学 en-keyword=HCV kn-keyword=HCV en-keyword=ATM kn-keyword=ATM en-keyword=Chk2 kn-keyword=Chk2 en-keyword=宿主因子 kn-keyword=宿主因子 en-keyword=DNA 損傷センサー kn-keyword=DNA 損傷センサー END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=5-2 article-no= start-page=2653 end-page=2659 dt-received= dt-revised= dt-accepted= dt-pub-year=1959 dt-pub=19590425 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=studies on the Pathogenic Agant of Infectious Hepatitis in Okayama Prefecture, Particularly on the Virus Isolated by the Embryonated Hen's Egg U: Characters of the Isolated Virus kn-title=岡山県に発生せる流行性肝炎病原体の研究特に孵化鶏卵に依り分離せるウイルスに就て 第2編 分離ウイルスの性状に就て en-subtitle= kn-subtitle= en-abstract= kn-abstract=The author studied the virological characters of the virus isolated by the Chick-embryo technic, and obtained the following results: Inoculation of the virus into the chorio-allantoic cavity of the 7 day old chick-embryo killed the chick-embryo on the 5th to 7th day after inoculation. The serial passage could be carried out by inoculation of the chorio-allantoic fluid or the chick-embryo liver, of which the latter gave a better result. The amniotic inoculation could kill the chick-embryo on the 4th to 5th day after inoculation, but LD(50) was lower than that by the chorio-allantoic route. The yalk sack inoculation could not give a good result. As for the distribution of the virus by chorio-allantoic inoculation, the virus could be best proved in the chick-embryo, particularly in the liver, the next in the chorio-allantoic fluid and very few in the other parts. The isolated virus easily passed Seitz E. K., Berkefeld N. and also Berkefeld W., though somewhat difficult through the last one; this fact suggests that the isolated virus is pretty small one. Though the infectious index of the virus to the chick-embryo varied with the generations of the passage, the average for 10 to 20 generations was 8.0. The isolated virus could be well preserved in the glycerin-salt solution. en-copyright= kn-copyright= en-aut-name=TawaraJutaro en-aut-sei=Tawara en-aut-mei=Jutaro kn-aut-name=俵寿太郎 kn-aut-sei=俵 kn-aut-mei=寿太郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部微生物学教室 END start-ver=1.4 cd-journal=joma no-vol=72 cd-vols= no-issue=1 article-no= start-page=229 end-page=234 dt-received= dt-revised= dt-accepted= dt-pub-year=1959 dt-pub=19591230 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the Pathogene of Infectious Hepatitis Part U Studies on the Hepatitis Virus being Parasitic on Single Free Cells kn-title=流行性肝炎の病原体に関する研究 第二編 遊離単一細胞を宿主とする肝炎ウイルスの研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Some properties of the hepatitis virus were reported already in part I. The author studied further the pathogenicity of the virus to single free cells. The virus used in this study was isolated from hepatitis patient and cultured in the chorio-allantoic cavity of chick embryo. and the following results were obtained. 1) The infection and the proliferation of the virus were scarcely found on various single free cells used in this study: this could be said especially in the case of EHRLICH's ascites tumor cells. The same findings were also obtained on the cultured L-cells. 2) The hepatitis virus used in this study caused the changes what could suppose as Cp-effect. This concept was thought to be valid, since this virus could cause almost identical degeneration of cells. Then, the virological properties of the virus, i.e. heat-ressistance, filtrability and resistance to ether, were studied again by the use of Cp.effect. And thers were found a fairly good coincidence of the resieults with the part I. en-copyright= kn-copyright= en-aut-name=SengokuAkihisa en-aut-sei=Sengoku en-aut-mei=Akihisa kn-aut-name=仙石晃久 kn-aut-sei=仙石 kn-aut-mei=晃久 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部微生物学教室 END start-ver=1.4 cd-journal=joma no-vol=86 cd-vols= no-issue=9-10 article-no= start-page=513 end-page=526 dt-received= dt-revised= dt-accepted= dt-pub-year=1974 dt-pub=19741030 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Virological Studies on Human Leukemia Report U. Immunofluorescent Detection of the Species-Specific (gs-1) Antigens and Interspecies-Specific (gs-3) Antigens in the Human Lymphoblastoid Cell Lines Chronically Infected with Rauscher Leukemia Virus kn-title=人白血病のウイルス学的研究 第2編 Rauscher白血病ウイルス感染人由来リンパ芽球様株細胞の蛍光抗体法によるspecies-specific(gs-1)antigenとinterspecies-specific(gs-3)antigenの検索 en-subtitle= kn-subtitle= en-abstract= kn-abstract=As a virological approach to the study of human leukemia, the group-specific (gs) antigens in the human lymphoblastoid cell lines chronically infected with Rauscher leukemia virus, OUMS-11a-R, OUMS-6C1-R1 and OUMS-6C1-R2, were examined by the immunofluorescence technique with anti-gs-1 rat serum and anti-gs-3 goat serum. Immunofluorescence-positive cells with the anti-Rauscher leukemia virus goat serum and anti-gs-1 rat serum were observed in 0.2-0.6% of OUMS-11a-R cells, and in 8-15% of OUMS-6C1-R1 and OUMS-6C1-R2 cells. However, no staining was detected in any cell lines with anti-gs-3 goat serum. The number of fluorescent cells roughly coincided with those of cells producing type-C virus particles as observed by electron microscopic examination. In all instances, the fluorescence was restricted to the cytoplasm. It was diffuse and homogeneous in almost all cases, although granular cytoplasmic fluorescence was sometimes observed. There was no nuclear or perinuclear fluorescence. The specificity of these antisera was confirmed by the occurrence of specific fluorescence in the spleen and liver of mice infected with Rauscher leukemia virus, but not in the control tests of uninfected mice. From these results of gs antigen analyses in the human lymphoblastoid cells chronically infected with Rauscher leukemia virus, it was considered that type-C virus particles propagated in these cells were Rauscher leukemia virus itself used for infection, and it seemed unlikely that the hypothetical viral genome of human origin was activated and human type-C virus particles were rescued. en-copyright= kn-copyright= en-aut-name=UnoJunichiro en-aut-sei=Uno en-aut-mei=Junichiro kn-aut-name=宇野潤一郎 kn-aut-sei=宇野 kn-aut-mei=潤一郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科 END start-ver=1.4 cd-journal=joma no-vol=86 cd-vols= no-issue=9-10 article-no= start-page=499 end-page=512 dt-received= dt-revised= dt-accepted= dt-pub-year=1974 dt-pub=19741030 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Virological Studies on Human Leukemia Report T. Analysis of Viral Antigens of Rauscher Murine Leukemia andHuman Leukemia Cells by Direct Immunofluorescence with Anti-Rauscher Leukemia Virus Serum kn-title=人白血病のウイルス学的研究 第1編 Rauscher白血病ウイルス抗血清を用いた蛍光抗体法によるRauscherマウス白血病細胞および人白血病細胞のウイルス抗原の検索 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Specificity of anti-Rauscher leukemia virus goat serum was strictly checked by purification, labelling with fluorescein and elimination of nonspecific reaction. Using this antiserum, antigen analyses of the spleen and liver cells of Rauscher leukemic mice and human leukemic cells were examined by the direct immunofluorescence technique and following results were obtained.By electron microscopy, the eclipse phase was reported to be about 1 week after virus inoculation, but it was found that viral antigen was observable already in three days after virus infection. In the experiment with human leukemias, cells from bone marrow or peripheral bloodsmears from patients with 20 acute leukemias (14 of myelocytic, 6 of lymphocytic), 6 chronic leukemias (3 of myelocytic, 3 of lymphocytic), 10 malignant lymphomas (4 of Hodgkin disease, 4 of lymphosarcoma, 2 of reticulum cell sarcoma), 2 multiple myeloma and 10 other disorders were tested with anti-Rauscher leukemia virus goat serum. However, specific fluorescence was not seen in any cells tested. Based on these findings, the role of virus in human leukemia was discussed. en-copyright= kn-copyright= en-aut-name=UnoJunichiro en-aut-sei=Uno en-aut-mei=Junichiro kn-aut-name=宇野潤一郎 kn-aut-sei=宇野 kn-aut-mei=潤一郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科 END start-ver=1.4 cd-journal=joma no-vol=102 cd-vols= no-issue=1-2 article-no= start-page=199 end-page=207 dt-received= dt-revised= dt-accepted= dt-pub-year=1990 dt-pub=199002 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Structural protein analysis of intracisternal A particles in adenovirus-induced mouse tumor kn-title=内在性小胞体内 A 粒子の構成蛋白に関する研究ーアデノウイルス12型誘発マウス腫瘍に認められた粒子についてー en-subtitle= kn-subtitle= en-abstract= kn-abstract=Analysis and purfication of structural proteins of intracisternal A particles produced in adenovirus-induced tumor were described. SDS-PAGE of purified intracisternal A particles demonstrated its major structural components, K92, K70 and K55, and minor components, K43 and K37. Two dimensional gel electrophoresis indicated a pI of K70 and K55 at 6.5 and 6.3, respectively, in the presence of sodium dodecyl sulfate. Purification of the main band, K70, in SDS-PAGE using reversed phase-HPLC was difficult in the standard acidic condition, but could be achieved in the neuttral condition. Although purificatin of K70 is generally difficult because of its hydrophobicity, the method shown here will be useful for furthey study of structural proteins of intracisternal A particles. en-copyright= kn-copyright= en-aut-name=HirakawaEiichiro en-aut-sei=Hirakawa en-aut-mei=Eiichiro kn-aut-name=平川栄一郎 kn-aut-sei=平川 kn-aut-mei=栄一郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=香川医科大学病理学講座第一病理学 en-keyword=小胞体内 A 粒子 kn-keyword=小胞体内 A 粒子 en-keyword=アデノウイルス誘発腫瘍 kn-keyword=アデノウイルス誘発腫瘍 en-keyword=構成蛋白分析 kn-keyword=構成蛋白分析 en-keyword=reversed phase-HPLC kn-keyword=reversed phase-HPLC END start-ver=1.4 cd-journal=joma no-vol=102 cd-vols= no-issue=1-2 article-no= start-page=143 end-page=152 dt-received= dt-revised= dt-accepted= dt-pub-year=1990 dt-pub=199002 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Integration and expression of E1 region DNA in human adenovirus type 12-induced tumors kn-title=ヒトアデノウィルス12型誘発腫瘍におけるE1領域遺伝子の組み込みと発現 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Integration and expression of human adenovirus type 12 (Ad12) were studied on two Ad12-induced tumor lines of C3Hf/OK mouse origin (IC and D tumors). Southern hybridization using whole Ad12 genome as probe demonstrated that DNA of IC and D tumors contained about 9 and 23 copies, respectively, of the entire Ad12 genome eqivalent per diploid cell. Left ends of Ad12 DNA appeared as off-size bands, indicating their linkage to different cellular DNAs. Southern hybridization using and Ad12 EcoRI-C fragment containing the E1 region as a probe revealed that intergration sites were much fewer than presumen numbers of integrated Ad12 genones. These results suggested that the viral and cellular DNA complex was repeated at integration sites. Northen hybridization using an Ad12 EcoRI-C fragment as a probe showed that tha E1 region was transcribed in both IC and D tumors. Much more intensive expression in the D tumor suggested possible dependence of the expression of the E1 region on the copy numbers of Ad12 genomes. en-copyright= kn-copyright= en-aut-name=MorikawaTomoko en-aut-sei=Morikawa en-aut-mei=Tomoko kn-aut-name=森川智子 kn-aut-sei=森川 kn-aut-mei=智子 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=香川医科大学病理学講座第一病理学 en-keyword=ヒトアデノウィルス12型 kn-keyword=ヒトアデノウィルス12型 en-keyword=E1領域 kn-keyword=E1領域 en-keyword=C3Hf/OK マウス kn-keyword=C3Hf/OK マウス en-keyword=ウィルス発癌 kn-keyword=ウィルス発癌 END start-ver=1.4 cd-journal=joma no-vol=103 cd-vols= no-issue=4 article-no= start-page=267 end-page=280 dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=1991 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hemadosorption phenomenon in cultured cells caused by HSV-1 induced Fc receptor : ultrastructural and biological studies kn-title=単純ヘルペスウイルス感染細胞表面に発現するFc-レセプターによる感作赤血球吸着反応―微細形態学的ならびに細胞生物学的考察― en-subtitle= kn-subtitle= en-abstract= kn-abstract=Adsorption of sensitized sheep erythrocytes to FL cells infected with HSV-1 was studied biologically and morphologically. Almost 100% of the FL cells at a late stage of infection (i.e. 23 hrs) were positive for the appearance of HSV-1 gC antigen, while about 86% of them had hemadsorption (HAD) activity. To elucidate why all the infected cells do not show HAD activity, FL cells at the similar stage of infection were examined by high-resolution scanning electron microscopy and also by immuno-scanning electron microscopy. When infected cells were treated first with peroxidase-antiperoxidase (PAP) rabbit IgG and then with goat anti-rabbit IgG Iabeled with colloidal gold, the surface of all the cells were clearly tagged with colloidal gold particles. Morphological observations of HAD revealed that many microvilli adhered to the surface of erythrocytes. Thus, in addition to the expression of HSV-induced FcR on the surface membrane of infected cells, which is prerequisite for HAD, microvilli play an essential role on the appearance of this phenomenon. en-copyright= kn-copyright= en-aut-name=BaiZeng-Liang en-aut-sei=Bai en-aut-mei=Zeng-Liang kn-aut-name=白増亮 kn-aut-sei=白 kn-aut-mei=増亮 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部ウイルス学教室 en-keyword=単純ヘルペスウイルス kn-keyword=単純ヘルペスウイルス en-keyword=Fc-レセプター kn-keyword=Fc-レセプター en-keyword=microvilli kn-keyword=microvilli en-keyword=hemadsorption kn-keyword=hemadsorption en-keyword=走査電子顕微鏡 kn-keyword=走査電子顕微鏡 END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=3-4 article-no= start-page=331 end-page=340 dt-received= dt-revised= dt-accepted= dt-pub-year=1992 dt-pub=1992 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Dectection of human papillomavirus genome in papillomas of head and neck region kn-title=頭頸部乳頭種病変におけるヒトパピロ−マウィルスの関与 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To investigate the etiological role of human papillomavirus (HPV), 14 cases of papillomas in head and neck region were examined virologically and clinicopathogically. Both dot blot and Southern blot hybridization methods were applied for HPV DNA detection. In all cases of multiple laryngeal papillomas, either HPV 6 (2 cases) or HPV 11 (2 cases) genomes were detected. The presence of the HPV genomes provides strong evidence for the HPV etiology of these laryngeal papilloma. In one case of sinonasal papilloma (exophytic type). HPV 6 DNA was detected. No HPV genome was found in the DNA from the remaining 4 sinonasal papillomas. However, their clincopathological findings suggested the viral etiology. No HPV genome was proved in 4 oral papillomas. Furthermore, neither clinical course nor histopathological findings suggested viral etiology. The sensitivity of blot hybridization (Vira probe HPV) in detecting HPV DNA was the same as that of Southern blot hybridization. en-copyright= kn-copyright= en-aut-name=KawakamiTakashi en-aut-sei=Kawakami en-aut-mei=Takashi kn-aut-name=川上登史 kn-aut-sei=川上 kn-aut-mei=登史 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部耳鼻咽喉科学教室 en-keyword=乳頭種 kn-keyword=乳頭種 en-keyword=Human Papillomavirus kn-keyword=Human Papillomavirus en-keyword=Dot Blot Hybridization kn-keyword=Dot Blot Hybridization en-keyword=Southern Blot Hybridization kn-keyword=Southern Blot Hybridization END start-ver=1.4 cd-journal=joma no-vol=103 cd-vols= no-issue=7-8 article-no= start-page=859 end-page=867 dt-received= dt-revised= dt-accepted= dt-pub-year=1991 dt-pub=199108 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Persistent herpes simplex virus type 2 infection in a hamster kidney cell line with a characteristic to grow at a high culture temperature kn-title=ハムスター腎臓由来株化細胞の高温馴化亜株における単純ヘルペスウイルス2型の持続感染 en-subtitle= kn-subtitle= en-abstract= kn-abstract=A subline of the baby hamster kidney cell line (BHK-21), which was adapted to grow at 41℃ and named BHK-21H, was used to examine the effect of pre-treatment of host cells with a high culture temperature on the growth of herpes simplex virus (HSV). BHK-21H cells were infected with HSV type 2 (HSV-2) at 41℃ and maintained for 7 days at the same temperature. When these cells were further cultivated after shift-down to 36℃, persistent infections were established. These infections were characterized by a carrier culture state ; the infected cultures were composed of infected and non-infected cells, and cell destruction and regrowth of cells caused a balanced state of culture. Two to 3 months after the establishment of the persistent infections, virus production in the cultures stopped spontaneously and colonial regrowth of uninfected cells was observed. A subline (BHK-21R) which was cured of the persistent infection was obtained. Cells of this subline showed resistance to reinfection of HSV. Persistent HSV-2 Infection was also established by pre-treatment of BHK-21H cells at 41℃ before virus infection and maintenance of the infected cultures at 36℃. These findings indicate that establishment of the persistent HSV-2 infection is mainly attributable to reduced permissiveness of BHK-21H cells for virus growth caused after heat treatment of the cells. en-copyright= kn-copyright= en-aut-name=KitamuraTetsuro en-aut-sei=Kitamura en-aut-mei=Tetsuro kn-aut-name=喜多村哲朗 kn-aut-sei=喜多村 kn-aut-mei=哲朗 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部小児科学教室 en-keyword=herpes simplex virus kn-keyword=herpes simplex virus en-keyword=persistent infection kn-keyword=persistent infection en-keyword=supraoptimal temperature kn-keyword=supraoptimal temperature en-keyword=carrier culture state kn-keyword=carrier culture state en-keyword=permissiveness kn-keyword=permissiveness END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=1-2 article-no= start-page=127 end-page=134 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=19930227 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on anti-HTLV-T antibody in interstitial lung diseases Part 2. Anti-HTLV-TIgG, IgM, and IgA antibodies in HTLV-T associated bronchiolo-alveolar disorder (HABA) kn-title=間質性肺疾患における抗 HTLV-T抗体に関する研究　第2編 HTLV-T関連細気管支･肺胞異常症 (HABA) における抗 HTLV-TIgG, IgM, IgA 抗体に関する検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To study the pathogenesis of HTLV-Tassociated bronchiolo-alveolar disorder (HABA), Western blot analysis was performed using MT-2 cell lysate antigens on the serum of 6 patients with HABA, 7 patients with adult T cell leukamia (ATL), 14 asymptomatic carriers and 9 healthy controls. Five(83%) of the 6 HABA patients were positive for anti-HTLV-T IgA antibodies, although all 7 ATL patients and 11 of the 14 asymptomatic carriers were negative. All HABA and ATL patients and asymptomatic carriers were positive for anti-HTLV-T IgG antibodies. Four(67%) of the 6 HABA patients, 2(29%) of the 7 ATL patients and 9(64%) of the 14 asymptomatic carriers were positive for anti-HTLV-T IgM antibodies. Statistically there was little difference in the incidences of anti-HTLV-T IgG and IgM antibodies among HABA and ATL patients and asymptomatic carriers, but the HABA patients showed a significantly higher incedence of IgA antibody than the ATL patients and asymptomatic carriers. Since specific IgA antibodies are produced in the local infected mucosa and part of the IgA antibodies are transferred into the serum, in conclusion, the anti-HTLV-T IgA antibodies in HABA patients reflect the localization of HTLV-T in lungs which play an important role in the pathogenesis of HABA. en-copyright= kn-copyright= en-aut-name=UenoKatsumi en-aut-sei=Ueno en-aut-mei=Katsumi kn-aut-name=植野克巳 kn-aut-sei=植野 kn-aut-mei=克巳 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=HTLV-T関連細気管支・肺胞異常症 kn-keyword=HTLV-T関連細気管支・肺胞異常症 en-keyword=抗 HTLV-TIgA 抗体 kn-keyword=抗 HTLV-TIgA 抗体 END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=1-2 article-no= start-page=119 end-page=126 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=19930227 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on anti-HTLV-T antibody in interstitial lung diseases Part 1. Western blot analysis for anti-HTLV-T antibody and HTLV-T related reaction in DBP and IIP kn-title=間質性肺疾患における抗 HTLV-T抗体に関する研究　第1編 DPB, IIPにおける抗 HTLV-T抗体並びに HTLV-T関連反応の Western blot 法による検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=By the immunofluorescent assay for the anti-HTLV-T antibody, the serum of many patients with diffuse panbronchiolitis (DBP) and idiopathic interstitial pneumonia (IIP) show two types of cytoplasmic fluorescence. One is a granular pattern in the MT-1 cell and diffuse pattern in the MT-2 cell. This is the typical pattern for the anti-HTLV-T antibody. The other is a diffuse pattern in the MT-1 and/or MT-2 cells. This pattern has been designated as HTLV-T related reaction. These serum reactions were investigated by Western blot analysis with an MT-2 cell lysate as antigen. Although about 20% of the patients with DBP and IIP were considered to be suffering from HTLV-T associated bronchiolo-alveolar disorder (HABA) because they showed the typical pattern of anti-HTLV-T antibody, only those patients with HABA were shown to have the antibodies against HTLV-T specific proteins (p19, p24, p28, pr53 and gp68). On the other hand, the patients with HTLV-T related reaction had neither the antibodies against any HTLV-T proteins nor the other protein components of MT-2. Thus, Western blot analysis revealed that antibodies against HTLV-T specific proteins were present only in the patients with HABA. en-copyright= kn-copyright= en-aut-name=UenoKatsumi en-aut-sei=Ueno en-aut-mei=Katsumi kn-aut-name=植野克巳 kn-aut-sei=植野 kn-aut-mei=克巳 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=びまん性汎細気管支炎 kn-keyword=びまん性汎細気管支炎 en-keyword=特発性間質性肺炎 kn-keyword=特発性間質性肺炎 en-keyword=HTLV-T抗体 kn-keyword=HTLV-T抗体 en-keyword=HTLV-T関連反応 kn-keyword=HTLV-T関連反応 en-keyword=Western blot 法 kn-keyword=Western blot 法 END start-ver=1.4 cd-journal=joma no-vol=113 cd-vols= no-issue=1 article-no= start-page=115 end-page=116 dt-received= dt-revised= dt-accepted= dt-pub-year=2001 dt-pub=20010428 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=新興感染症 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=山田雅夫 kn-aut-sei=山田 kn-aut-mei=雅夫 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部ウイルス学講座 END start-ver=1.4 cd-journal=joma no-vol=114 cd-vols= no-issue=3 article-no= start-page=275 end-page=281 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=20030131 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Long-term prognosis of the chronic hepatitis C patients with interferon: Comparison among virological responders, biochemical responders and non-responders kn-title=インターフェロン治療後C型慢性肝炎患者の長期予後　―ウイルス学的著効例，生化学的著効例と無効例の比較― en-subtitle= kn-subtitle= en-abstract= kn-abstract=To evaluate the prognosis of the sustained biochemical responder after interferon (IFN) therapy, we retrospectively studied 252 chronic hepatitis C patients who were treated with IFN. Patients were divided into four groups: group A, sustained virological responders (n=84); group B,sustained biochemical but not virological responders (n=43); group C, incomplete responders (n=64); group D, non responders (n=61). The levels of several liver function tests were evaluated at the end of the observation period (4.2±1.6 years, mean±SD) compared with those at just before IFN therapy. The levels of cholinesterase, albumin, γ-globulin, zinc sufate turbidity test, platelet count and clearance rate of indocyanine green test improved in group A (p<0.05), became worse in group D (p<0.05) and did not change in group B. The incidence of hepatocellular carcinoma was significantly higher in group D than in group B (p<0.01);Kaplan-Meier method, log-rank test). The hazard ratio for hapatocarcinogenesis of the patients in group A and B was significantly lower than that in group C and D (hazard ratio: 0.27, range of 0.08-0.98; p=0.046) adjusted for age, gender, stage and total alcohol consumption. These results suggest that the progress of liver disease and liver carcinogenesis was more suppressed in sustained biochemical responders than in non reponders. en-copyright= kn-copyright= en-aut-name=MiyakeMasanobu en-aut-sei=Miyake en-aut-mei=Masanobu kn-aut-name=三宅正展 kn-aut-sei=三宅 kn-aut-mei=正展 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry en-keyword=C型肝炎 kn-keyword=C型肝炎 en-keyword=インターフェロン kn-keyword=インターフェロン en-keyword=生化学的持続著効 kn-keyword=生化学的持続著効 END start-ver=1.4 cd-journal=joma no-vol=117 cd-vols= no-issue=3 article-no= start-page=219 end-page=224 dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=20060104 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Characterization and usefulness of a monoclonal antibody against human herpesvirus-7 DNA polymerase processivity factor kn-title=ヒトヘルペスウイルス7型のDNA ポリメラーゼサブユニットに対する単クローン抗体の性状と有用性 en-subtitle= kn-subtitle= en-abstract= kn-abstract=A monoclonal antibody (MAb), IK17, was developed and found useful for the analysis of human herpesvirus-7 (HHV7) genome replication. In Western blot analysis, the MAb IK17 specifically detected an HHV7 DNA polymerase subunit,U27 protein,expressed in both Escherichia coli (E.Coli)and HHV7-infected cells.Analysis by the same method of truncated U27 proteins expressed in E. Coli demonstrated that the MAb IK17 recognizes an epitope between amino acid 1 and 133 of the U27 protein.The indirect immunofluorescence (IF)method with MAb IK17 detected an unexpected reduction of U27 protein in the infected cells that were treated with a viral DNA polymerase inhibitor,phosphonoacetic acid (PAA),although no reduction of U27 mRNA was observed in the cells by Northern blot analysis. The data suggest the possible usefulness of the MAb IK17 for obtaining clues to characterize an unknown feature of the U27 protein. Immunoprecipitation experiments with the MAb IK17 enabled to detect at least four U27 protein-associated phosphorylated polypeptides in addition to the U27 protein itself.The result indicates the usefulness of the MAb IK17 for qualitative and quantitative analysis of the U27 proteinassociated viral and cellular factors. These analyses contribute to elucidation of the HHV7 genome replication system. en-copyright= kn-copyright= en-aut-name=NambaHikaru en-aut-sei=Namba en-aut-mei=Hikaru kn-aut-name=難波ひかる kn-aut-sei=難波 kn-aut-mei=ひかる aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病原ウイルス学 en-keyword=ヒトヘルペスウイルス7型 (Human Herpesvirus-7) kn-keyword=ヒトヘルペスウイルス7型 (Human Herpesvirus-7) en-keyword=DNA polymerase processivity factor kn-keyword=DNA polymerase processivity factor en-keyword=単クローン抗体 (monoclonal antibody) kn-keyword=単クローン抗体 (monoclonal antibody) END start-ver=1.4 cd-journal=joma no-vol=117 cd-vols= no-issue=1 article-no= start-page=85 end-page=86 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050520 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ノロウイルス en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=小倉肇 kn-aut-sei=小倉 kn-aut-mei=肇 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山県環境保健センター END start-ver=1.4 cd-journal=joma no-vol=120 cd-vols= no-issue=1 article-no= start-page=29 end-page=34 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080501 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Statins inhibit hepatitis C virus RNA replication in human hepatoma cells kn-title=培養肝細胞を用いたスタチン剤のＣ型肝炎ウイルス抑制効果について en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=IkedaMasanori en-aut-sei=Ikeda en-aut-mei=Masanori kn-aut-name=池田正徳 kn-aut-sei=池田 kn-aut-mei=正徳 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　分子生物学 en-keyword=HCV kn-keyword=HCV en-keyword=レプリコン kn-keyword=レプリコン en-keyword=スタチン kn-keyword=スタチン en-keyword=HMG-CoA reductase kn-keyword=HMG-CoA reductase en-keyword=ゲラニルゲラニル化 kn-keyword=ゲラニルゲラニル化 END