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ID 53335
JaLCDOI
フルテキストURL
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著者
Hiramoto, Hiroki Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Dansako, Hiromichi Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takeda, Midori Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Satoh, Shinya Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Wakita, Takaji Department of Virology II, National Institute of Infectious Disease
Ikeda, Masanori Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kato, Nobuyuki Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
抄録
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.
キーワード
HCV
annexin A1
Li23 cell line
Li23-derived D7 cells
HCV-JFH-1
Amo Type
Original Article
発行日
2015-04
出版物タイトル
Acta Medica Okayama
69巻
2号
出版者
Okayama University Medical School
開始ページ
71
終了ページ
78
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
著作権者
CopyrightⒸ 2015 by Okayama University Medical School
論文のバージョン
publisher
査読
有り
PubMed ID
Web of Sience KeyUT