Gokhale Nandan S, Vazquez Christine, Horner Stacy M
Department of Molecular Genetics & Microbiology, Duke University Medical Center, Durham, NC 27710.
Department of Molecular Genetics & Microbiology, Duke University Medical Center, Durham, NC 27710 ; Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Future Virol. 2014;9(12):1061-1075. doi: 10.2217/fvl.14.89.
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.
丙型肝炎病毒(HCV)可引发慢性肝病,在全球范围内构成重大的临床和经济负担。HCV是一种RNA病毒,在受感染的肝脏中被宿主模式识别受体识别为非自身物质,从而触发下游向干扰素(IFN)的信号传导。III型干扰素在针对HCV的免疫中发挥重要作用,其基因位点的人类遗传变异与不同的HCV感染结果相关。HCV逃避宿主抗病毒先天性免疫反应,以介导肝脏中的持续感染。本综述聚焦于抗HCV先天性免疫感应、先天性信号传导和效应器,以及HCV用于逃避和调节宿主先天性免疫的过程和蛋白质。