Hepatitis C virus: evasion of the interferon-induced antiviral response.
Hepatitis C virus (HCV) is an emerging virus of great medical significance. A low drug-response rate and a high frequency of persistent infection have caused HCV to reach pandemic proportions. Many infected individuals go on to develop liver cirrhosis and hepatocellular carcinoma, and HCV is now the leading reason for liver transplants in the United States. Differences in genotype response to interferon therapy suggests that one or more viral genes may participate in evasion of the interferon-mediated cellular antiviral response. This review focuses on the viral genes that interact with the host cell to evade the interferon response and on the insights that these interactions may provide into HCV pathogenesis.
University of Southern California, Department of Molecular Microbiology and Immunology, Los Angeles, CA 90089, USA.
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D000998:Antiviral Agents / Q000494:pharmacology*; D005814:Genes, Viral / Q000187:drug effects; D016174:Hepacivirus / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D006526:Hepatitis C / Q000209:etiology*; D006801:Humans; D007372:Interferons / Q000494:pharmacology*; D014759:Viral Envelope Proteins / Q000378:metabolism; D017361:Viral Nonstructural Proteins; D019892:eIF-2 Kinase / Q000378:metabolism; D012324:RNA-Dependent RNA Polymerase
D000998:Antiviral Agents; D007372:Interferons; D014759:Viral Envelope Proteins; D017361:Viral Nonstructural Proteins; D019892:eIF-2 Kinase; C091015:glycoprotein E2, Hepatitis C virus; C087036:NS-5 protein, hepatitis C virus; D012324:RNA-Dependent RNA Polymerase