Innate immune escape by Dengue and West Nile viruses

被引：61

作者：

Gack, Michaela U. ^{[1
]}

Diamond, Michael S. ^{[2
,3
,4
,5
]}

机构：

[1] Univ Chicago, Dept Microbiol, Chicago, IL 60637 USA

[2] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA

[3] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[4] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA

[5] Washington Univ, Sch Med, Ctr Human Immunol & Immunotherapy Programs, St Louis, MO 63110 USA

来源：

CURRENT OPINION IN VIROLOGY | 2016年 / 20卷

基金：

美国国家卫生研究院;

关键词：

RIG-I; ALPHA/BETA-INTERFERON; MESSENGER-RNA; 3-DIMENSIONAL ARCHITECTURE; IMMUNOLOGICAL BEHAVIOR; VIRAL EVASION; INFECTION; REPLICATION; PROTEIN; MDA5;

D O I：

10.1016/j.coviro.2016.09.013

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Dengue (DENV) and West Nile (WNV) viruses are mosquito transmitted flaviviruses that cause significant morbidity and mortality worldwide. Disease severity and pathogenesis of DENV and WNV infections in humans depend on many factors, including pre-existing immunity, strain virulence, host genetics and virus-host interactions. Among the flavivirus-host interactions, viral evasion of type I interferon (IFN)-mediated innate immunity has a critical role in modulating pathogenesis. DENV and WNV have evolved effective strategies to evade immune surveillance pathways that lead to IFN induction and to block signaling downstream of the IFN-alpha/beta receptor. Here, we discuss recent advances in our understanding of the molecular mechanisms by which DENV and WNV antagonize the type I IFN response in human cells.

引用

页码：119 / 128

页数：10

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