The Regulatory Network of Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway in Viral Evasion

被引:11
|
作者
Hu, Tongyu [1 ]
Pan, Mingyu [1 ]
Yin, Yue [1 ]
Wang, Chen [1 ]
Cui, Ye [2 ,3 ]
Wang, Quanyi [1 ]
机构
[1] China Pharmaceut Univ, Dept Life Sci & Technol, State Key Lab Nat Med, Nanjing, Peoples R China
[2] Boston Childrens Hosp, Div Immunol, Boston, MA 02115 USA
[3] Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA
基金
中国国家自然科学基金;
关键词
viral evasion; cGAS-STING; type I interferon; innate immune; post-translational modification; ANTIVIRAL RESPONSE; DNA SENSOR; CGAS; UBIQUITINATION; ACTIVATION; PROTEIN; IMMUNITY; TBK1; SARS; INHIBITION;
D O I
10.3389/fmicb.2021.790714
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Virus infection has been consistently threatening public health. The cyclic GMP-AMP synthase (cGAS)-Stimulator of Interferon Genes (STING) pathway is a critical defender to sense various pathogens and trigger innate immunity of mammalian cells. cGAS recognizes the pathogenic DNA in the cytosol and then synthesizes 2 ' 3 '-cyclic GMP-AMP (2 ' 3 ' cGAMP). As the second messenger, cGAMP activates STING and induces the following cascade to produce type I interferon (IFN-I) to protect against infections. However, viruses have evolved numerous strategies to hinder the cGAS-STING signal transduction, promoting their immune evasion. Here we outline the current status of the viral evasion mechanism underlying the regulation of the cGAS-STING pathway, focusing on how post-transcriptional modifications, viral proteins, and non-coding RNAs involve innate immunity during viral infection, attempting to inspire new targets discovery and uncover potential clinical antiviral treatments.
引用
收藏
页数:14
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