title: Hepatitis C Virus. Strategies to Evade Antiviral Responses.
abstract: Hepatitis C virus (HCV) causes chronic liver disease and poses a major clinical and economic burden worldwide. HCV is an RNA virus that is sensed as non-self in the infected liver by host pattern recognition receptors, triggering downstream signaling to interferons (IFNs). The type III IFNs play an important role in immunity to HCV, and human genetic variation in their gene loci is associated with differential HCV infection outcomes. HCV evades host antiviral innate immune responses to mediate a persistent infection in the liver. This review focuses on anti-HCV innate immune sensing, innate signaling and effectors, and the processes and proteins used by HCV to evade and regulate host innate immunity.
authors.affiliation: Department of Molecular Genetics & Microbiology, Duke University Medical Center, Durham, NC 27710.
authors.forename: Nandan S
authors.initials: NS
authors.lastname: Gokhale
authors.affiliation: Department of Molecular Genetics & Microbiology, Duke University Medical Center, Durham, NC 27710.
authors.forename: Christine
authors.initials: C
authors.lastname: Vazquez
authors.affiliation: Department of Molecular Genetics & Microbiology, Duke University Medical Center, Durham, NC 27710 ; Department of Medicine, Duke University Medical Center, Durham, NC 27710.
authors.forename: Stacy M
authors.initials: SM
authors.lastname: Horner
keywords: HCV; IFN; ISGs; Immune Evasion; MAVS; NS3/4A; RIG-I