Innate immunity and hepatitis C virus: eluding the host cell defense.
Interferon-alpha (IFN-alpha) mono-therapy is largely ineffective for most of the hepatitis C virus (HCV)-infected patients that receive it. The addition of ribavirin to IFN therapy has increased the response rate dramatically. While many factors are implicated in determining the success rate for IFN therapy, viral genotype seems to play a crucial role. Examining differences in viral gene sequences has and will continue to advance our understanding as to how HCV and other viruses circumvent the IFN response. Here we review the different ways that HCV evades the immune response elicited by IFN.
Taylor
Deborah R
DR
Laboratory of Hepatitis and Related Emerging Agents, Division of Emerging and Transfusion-Transmitted Diseases, Office of Blood Research and Review, CBER FDA, Bethesda, MD 20892, USA. Deborah.Taylor@FDA.HHS.gov
Silberstein
Erica
E
D015088:2',5'-Oligoadenylate Synthetase / Q000378:metabolism; D000243:Adenosine Deaminase / Q000502:physiology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D006526:Hepatitis C / Q000235:genetics / Q000276:immunology / Q000628:therapy; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000276:immunology; D018448:Models, Immunological; D009569:Nitric Oxide / Q000378:metabolism; D016601:RNA-Binding Proteins; D053633:Receptor, Interferon alpha-beta / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D014764:Viral Proteins / Q000276:immunology; D019892:eIF-2 Kinase / Q000378:metabolism
D000949:Histocompatibility Antigens Class II; C507964:IFNAR1 protein, human; D016601:RNA-Binding Proteins; D014764:Viral Proteins; D053633:Receptor, Interferon alpha-beta; D009569:Nitric Oxide; D007372:Interferons; D019892:eIF-2 Kinase; D015088:2',5'-Oligoadenylate Synthetase; C567955:ADARB1 protein, human; D000243:Adenosine Deaminase