No Love Lost Between Viruses and Interferons

被引：121

作者：

Fensterl, Volker ^{[1
]}

Chattopadhyay, Saurabh ^{[1
]}

Sen, Ganes C. ^{[1
]}

机构：

[1] Cleveland Clin, Lerner Res Inst, Dept Mol Genet, Cleveland, OH 44195 USA

来源：

ANNUAL REVIEW OF VIROLOGY, VOL 2 | 2015年 / 2卷

基金：

美国国家卫生研究院;

关键词：

virus infection; innate immunity; interferon-stimulated gene; pathogenesis; antiviral action; viral evasion; dsRNA; pattern-recognition receptor; interferon-lambda; TOLL-LIKE RECEPTOR-3; DOUBLE-STRANDED-RNA; HEPATITIS-C VIRUS; INFLUENZA-A VIRUS; NF-KAPPA-B; PLASMACYTOID DENDRITIC CELLS; MURINE NOROVIRUS INFECTION; PERSISTENT LCMV INFECTION; IFIT FAMILY-MEMBERS; INDUCIBLE GENE-I;

D O I：

10.1146/annurev-virology-100114-055249

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The interferon system protects mammals against virus infections. There are several types of interferons, which are characterized by their ability to inhibit virus replication and resultant pathogenesis by triggering both innate and cell-mediated immune responses. Virus infection is sensed by a variety of cellular pattern-recognition receptors and triggers the synthesis of interferons, which are secreted by the infected cells. In uninfected cells, cell surface receptors recognize the secreted interferons and activate intracellular signaling pathways that induce the expression of interferon-stimulated genes; the proteins encoded by these genes inhibit different stages of virus replication. To avoid extinction, almost all viruses have evolved mechanisms to defend themselves against the interferon system. Consequently, a dynamic equilibrium of survival is established between the virus and its host, an equilibrium that can be shifted to the host's favor by the use of exogenous interferon as a therapeutic antiviral agent.

引用

页码：549 / 572

页数：24

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