Abstract
The purpose of this study was to elucidate the mechanism behind low efficacy of interferon therapy to hepatitis C virus infected patients by using primary monkey hepatic parenchymal cells as a surrogate of primary human liver cells. The effects of various cytokines on the antiviral activity of IFNs in the monkey hepatic cells were studied to search for physiological inhibitors. Interleukin-1 alpha, EGF, and HGF showed suppressive effects on the antiviral activity of IFN-alpha, -beta in primary monkey hepatic cells when examined by the yield reduction method using vesicular stomatitis virus (VSV). In contrast, 50 ng/ml of TNF and IL-6 had no suppressive effect on the IFN-induced antiviral state in the hepatic cells.
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