title: Innate immune responses in hepatitis C virus infection.
abstract: Hepatitis C virus (HCV) is a major causative agent of chronic hepatitis and hepatocellular carcinoma worldwide and thus poses a significant public health threat. A hallmark of HCV infection is the extraordinary ability of the virus to persist in a majority of infected people. Innate immune responses represent the front line of defense of the human body against HCV immediately after infection. They also play a crucial role in orchestrating subsequent HCV-specific adaptive immunity that is pivotal for viral clearance. Accumulating evidence suggests that the host has evolved multifaceted innate immune mechanisms to sense HCV infection and elicit defense responses, while HCV has developed elaborate strategies to circumvent many of these. Defining the interplay of HCV with host innate immunity reveals mechanistic insights into hepatitis C pathogenesis and informs approaches to therapy. In this review, we summarize recent advances in understanding innate immune responses to HCV infection, focusing on induction and effector mechanisms of the interferon antiviral response as well as the evasion strategies of HCV.
authors.affiliation: Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA.
authors.forename: Kui
authors.initials: K
authors.lastname: Li
authors.forename: Stanley M
authors.initials: SM
authors.lastname: Lemon
mesh_terms: D016174:Hepacivirus / Q000276:immunology*; D006526:Hepatitis C / Q000276:immunology* / Q000821:virology; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D007372:Interferons / Q000276:immunology; D018168:Receptors, Retinoic Acid / Q000378:metabolism; D051196:Toll-Like Receptor 3 / Q000378:metabolism
chemical_list: C437968:PLAAT4 protein, human; D018168:Receptors, Retinoic Acid; C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3; D007372:Interferons