Mechanisms of Antiviral Immune Evasion of SARS-CoV-2

Daniel K Beyer; Adriana Forero

doi:10.1016/j.jmb.2021.167265

Mechanisms of Antiviral Immune Evasion of SARS-CoV-2

J Mol Biol. 2022 Mar 30;434(6):167265. doi: 10.1016/j.jmb.2021.167265. Epub 2021 Sep 22.

Authors

Daniel K Beyer¹, Adriana Forero²

Affiliations

¹ Molecular Genetics, College of Arts and Sciences, The Ohio State University, Columbus, OH 43210, USA.
² Department of Microbial Infection and Immunity, College of Medicine, The Ohio State University, Columbus, OH 43210, USA. Electronic address: adriana.forero@osumc.edu.

Abstract

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.

Keywords: COVID-19; ISGs; SARS-CoV-2; immune evasion; interferons.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

COVID-19* / genetics
COVID-19* / immunology
Gene Expression
Humans
Immune Evasion*
Immunity, Innate
Interferons* / genetics
RNA, Viral / immunology
SARS-CoV-2* / immunology

Substances

RNA, Viral
Interferons