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HCV replication was significantly inhibited by SAHA at concentrations below 1\u2009\u03bcM with no cellular toxicity. Another HDAC inhibitor, tricostatin A, also showed reduction of HCV replication. The microarray analysis and quantitative RT\u2010PCR demonstrated up\u2010regulation of <jats:italic>osteopontin<\/jats:italic> (<jats:italic>OPN<\/jats:italic>) and down\u2010regulation of <jats:italic>apolipoprotein\u2010A1<\/jats:italic> (<jats:italic>Apo\u2010A1<\/jats:italic>) after SAHA treatment. Direct gene induction of <jats:italic>OPN<\/jats:italic> and knockdown of <jats:italic>Apo\u2010A1<\/jats:italic> also showed reduction of HCV replication. The liver specific <jats:italic>microRNA\u2010122<\/jats:italic>, which is involved in HCV replication, was not affected by SAHA treatment. These results suggest that SAHA has suppressive effect on HCV replication through alterations of gene expression such as <jats:italic>OPN<\/jats:italic> and <jats:italic>Apo\u2010A1<\/jats:italic> in host cells. Epigenetic treatment with HDAC inhibitors may be a novel therapeutic approach for diseases associated with HCV infection such as chronic hepatitis, liver cirrhosis, and HCC. J. Cell. 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