| Literature DB >> 25983854 |
Nandan S Gokhale1, Christine Vazquez1, Stacy M Horner2.
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.Entities:
Keywords: HCV; IFN; ISGs; Immune Evasion; MAVS; NS3/4A; RIG-I
Year: 2014 PMID: 25983854 PMCID: PMC4430848 DOI: 10.2217/fvl.14.89
Source DB: PubMed Journal: Future Virol ISSN: 1746-0794 Impact factor: 1.831