Viral evasion of intracellular DNA and RNA sensing

被引:407
作者
Chan, Ying Kai [1 ]
Gack, Michaela U. [2 ]
机构
[1] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA
[2] Univ Chicago, Dept Microbiol, Chicago, IL 60637 USA
基金
美国国家卫生研究院;
关键词
INNATE IMMUNE-RESPONSE; DOUBLE-STRANDED-RNA; HEPATITIS-C-VIRUS; CYCLIC GMP-AMP; ANTIVIRAL SIGNALING PROTEIN; PARAMYXOVIRUS V PROTEINS; PAPAIN-LIKE PROTEASE; I-LIKE RECEPTORS; SENSOR RIG-I; CYTOSOLIC DNA;
D O I
10.1038/nrmicro.2016.45
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
The co-evolution of viruses with their hosts has led to the emergence of viral pathogens that are adept at evading or actively suppressing host immunity. Pattern recognition receptors (PRRs) are key components of antiviral immunity that detect conserved molecular features of viral pathogens and initiate signalling that results in the expression of antiviral genes. In this Review, we discuss the strategies that viruses use to escape immune surveillance by key intracellular sensors of viral RNA or DNA, with a focus on RIG-I-like receptors (RLRs), cyclic GMP-AMP synthase (cGAS) and interferon-gamma (IFN gamma)-inducible protein 16 (IFI16). Such viral strategies include the sequestration or modification of viral nucleic acids, interference with specific post-translational modifications of PRRs or their adaptor proteins, the degradation or cleavage of PRRs or their adaptors, and the sequestration or relocalization of PRRs. An understanding of viral immune-evasion mechanisms at the molecular level may guide the development of vaccines and antivirals.
引用
收藏
页码:360 / 373
页数:14
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