Premium
Griseofulvin, an oral antifungal agent, suppresses hepatitis C virus replication in vitro
Author(s) -
Jin Haofan,
Yamashita Atsuya,
Maekawa Shinya,
Yang Pinting,
He Limin,
Takayanagi Satoru,
Wakita Takaji,
Sakamoto Naoya,
Enomoto Nobuyuki,
Ito Masahiko
Publication year - 2008
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2008.00352.x
Subject(s) - griseofulvin , ribavirin , virology , subgenomic mrna , replicon , hepatitis c virus , interferon , internal ribosome entry site , virus , biology , in vitro , medicine , rna , ribosome , gene , biochemistry , pathology , plasmid
Aim: Hepatitis C virus (HCV), which infects an estimated 170 million people worldwide, is a major cause of chronic liver disease. The current standard therapy for chronic hepatitis C is based on pegylated interferon (IFN)α in combination with ribavirin. However, the success rate remains at approximately 50%. Therefore, alternative agents are needed for the treatment of HCV infection. Methods: Using an HCV‐1b subgenomic replicon cell culture system (Huh7/Rep‐Feo), we found that griseofulvin, an oral antifungal agent, suppressed HCV‐RNA replication and protein expression in a dose‐dependent manner. We also found that griseofulvin suppressed the replication of infectious HCV JFH‐1. A combination of IFNα and griseofulvin exhibited a synergistic inhibitory effect in Huh7/Rep‐Feo cells. Results: We found that griseofulvin blocked the cell cycle at the G 2 /M phase in the HCV subgenomic replicon cells, but did not inhibit HCV internal ribosome entry site‐dependent translation. Conclusion: Our results suggest that griseofulvin may represent a new approach to the development of a novel therapy for HCV infection.