Regulation of hepatic innate immunity by hepatitis C virus

被引：222

作者：

Horner, Stacy M. ^{[1
]}

Gale, Michael, Jr. ^{[1
]}

机构：

[1] Univ Washington, Dept Immunol, Seattle, WA 98195 USA

来源：

NATURE MEDICINE | 2013年 / 19卷 / 07期

关键词：

INTERFERON-STIMULATED GENES; ANTIVIRAL SIGNALING PROTEIN; RIG-I; ADAPTER PROTEIN; MEMBRANE ASSOCIATION; RIBAVIRIN THERAPY; NS3/4A PROTEASE; INTERLEUKIN; 28B; ISG EXPRESSION; IL28B;

D O I：

10.1038/nm.3253

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Hepatitis C virus (HCV) is a global public health problem involving chronic infection of the liver, which can cause liver disease and is linked with liver cancer. Viral innate immune evasion strategies and human genetic determinants underlie the transition of acute HCV infection to viral persistence and the support of chronic infection. Host genetic factors, such as sequence polymorphisms in IFNL3, a gene in the host interferon system, can influence both the outcome of the infection and the response to antiviral therapy. Recent insights into how HCV regulates innate immune signaling within the liver reveal a complex interaction of patient genetic background with viral and host factors of innate immune triggering and control that imparts the outcome of HCV infection and immunity.

引用

页码：879 / 888

页数：10

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