Interferons Specifically Suppress the Translation from the Internal Ribosome Entry Site of Hepatitis C Virus through a Double‐Stranded RNA–Activated Protein Kinase–Independent Pathway

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Abstract
Interferon (IFN) therapy is used worldwide as the best available treatment for hepatitis C virus (HCV) infection; however, little is known about how IFN or other drugs work against liver diseases. The effect of 6 drugs (glycyrrhizin, ursodeoxycholic acid, ribavirin, methylprednisolone, IFN-α, and IFN-β) on HCV RNA translation from the HCV internal ribosome entry site (IRES) was investigated, using a bicistronic reporter containing the HCV IRES. IFNs suppressed both cap-dependent and HCV IRES–dependent translation, with HCV IRES–dependent translation being more significantly suppressed. In contrast to HCV IRES, IFN did not suppress either foot-and-mouth disease virus IRES–dependent or encephalomyocarditis virus IRES–dependent translation more than it suppressed cap-dependent translation. Moreover, dominant inhibition of HCV IRES–dependent over cap-dependent translation depended neither on the double-stranded RNA–activated protein kinase activation nor on La protein function. These results indicate a novel antiviral effect of IFNs against HCV

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