ID 53335
JaLCDOI
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Author
Hiramoto, Hiroki
Takeda, Midori
Satoh, Shinya
Wakita, Takaji
Ikeda, Masanori
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.
Keywords
HCV
annexin A1
Li23 cell line
Li23-derived D7 cells
HCV-JFH-1
Amo Type
Original Article
Published Date
2015-04
Publication Title
Acta Medica Okayama
Volume
volume69
Issue
issue2
Publisher
Okayama University Medical School
Start Page
71
End Page
78
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2015 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Science KeyUT