Mechanisms of Antiviral Immune Evasion of SARS-CoV-2

被引：71

作者：

Beyer, Daniel ^{[1
]}

Forero, Adriana ^{[2
]}

机构：

[1] Ohio State Univ, Coll Arts & Sci, Mol Genet, Columbus, OH 43210 USA

[2] Ohio State Univ, Coll Med, Dept Microbial Infect & Immun, Columbus, OH 43210 USA

来源：

JOURNAL OF MOLECULAR BIOLOGY | 2022年 / 434卷 / 06期

关键词：

PAPAIN-LIKE PROTEASE; E3 UBIQUITIN LIGASE; I INTERFERON; NUCLEAR IMPORT; RNA; INFECTION; MDA5; RECOGNITION; ACTIVATION; RESPONSES;

D O I：

10.1016/j.jmb.2021.167265

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is characterized by a delayed interferon (IFN) response and high levels of proinflammatory cytokine expression. Type I and III IFNs serve as a first line of defense during acute viral infections and are readily antagonized by viruses to establish productive infection. A rapidly growing body of work has interrogated the mechanisms by which SARS-CoV-2 antagonizes both IFN induction and IFN signaling to establish productive infection. Here, we summarize these findings and discuss the molecular interactions that prevent viral RNA recognition, inhibit the induction of IFN gene expression, and block the response to IFN treatment. We also describe the mechanisms by which SARS-CoV-2 viral proteins promote host shutoff. A detailed understanding of the host-pathogen interactions that unbalance the IFN response is critical for the design and deployment of host-targeted therapeutics to manage COVID-19. (c) 2021 Elsevier Ltd. All rights reserved.

引用

页数：15

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