Induction and evasion of innate antiviral responses by hepatitis C virus.
Persistent hepatitis C virus infection is associated with progressive hepatic fibrosis and liver cancer. Acute infection evokes several distinct innate immune responses, but these are partially or completely countered by the virus. Hepatitis C virus proteins serve dual functions in replication and immune evasion, acting to disrupt cellular signaling pathways leading to interferon synthesis, subvert Jak-STAT signaling to limit expression of interferon-stimulated genes, and block antiviral activities of interferon-stimulated genes. The net effect is a multilayered evasion of innate immunity, which negatively influences the subsequent development of antigen-specific adaptive immunity, thereby contributing to virus persistence and resistance to therapy.
Lemon
Stanley M
SM
Division of Infectious Disease, Department of Medicine, Center for Translational Immunology, Inflammatory Diseases Institute, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7030, USA.
D000818:Animals; D016174:Hepacivirus / Q000276:immunology*; D006526:Hepatitis C / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D008099:Liver / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000821:virology; D015398:Signal Transduction / Q000276:immunology
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