Volume 38, Issue 5 p. 1282-1288
Original Article
Free Access

Cyclosporin A suppresses replication of hepatitis C virus genome in cultured hepatocytes

Koichi Watashi

Koichi Watashi

Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan

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Makoto Hijikata

Makoto Hijikata

Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan

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Masahiro Hosaka

Masahiro Hosaka

Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan

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Masashi Yamaji

Masashi Yamaji

Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan

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Kunitada Shimotohno Ph.D.

Corresponding Author

Kunitada Shimotohno Ph.D.

Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kyoto, Japan

Department of Viral Oncology, Institute for Virus Research, Kyoto University, Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. fax: (81) 75-751-3998===Search for more papers by this author
First published: 30 December 2003
Citations: 430

Abstract

Persistent infection of hepatitis C virus (HCV) is a major cause of liver diseases such as chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Searching for a substance with anti-HCV potential, we examined the effects of a variety of compounds on HCV replication using a HCV subgenomic replicon cell culture system. Consequently, the immunosuppressant cyclosporin A (CsA) was found to have a suppressive effect on the HCV replicon RNA level and HCV protein expression in these cells. CsA also inhibited multiplication of the HCV genome in a cultured human hepatocyte cell line infected with HCV using HCV-positive plasma. This anti-HCV activity of CsA appeared to be independent of its immunosuppressive function. In conclusion, our results suggest that CsA may represent a new approach for the development of anti-HCV therapy.