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Review
. 2020 Dec;40(12):543-548.
doi: 10.1089/jir.2020.0214.

Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2

Hongjie Xia  1 , Pei-Yong Shi  1   2   3   4
Affiliations
Review

Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2

Hongjie Xia et al. J Interferon Cytokine Res. 2020 Dec.

Abstract

The coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), warranting urgent study of the molecular mechanisms of SARS-CoV-2 infection and host immune response. Type I interferon (IFN-I) is a key component of host innate immune system responsible for eliminating the virus at the early stage of infection. In contrast, SARS-CoV-2 has evolved multiple strategies to evade innate immune response to facilitate viral replication, transmission, and pathogenesis. This review summarizes the recent progresses on SARS-CoV-2 proteins that antagonize host IFN-I production and/or signaling. These progresses have provided knowledge for new vaccine and antiviral development to prevent and control COVID-19.

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

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Conflict of interest statement

No competing financial interests exist.

Figures

FIG. 1.
FIG. 1.
SARS-CoV-2 proteins antagonize host IFN-I response. (A) Genome structure of SARS-CoV-2. The opening reading frames are shown, including ORF1ab (nonstructural proteins), structural proteins, and accessory proteins. (B) Evasion of IFN-I by SARS-CoV-2 proteins. The inhibitory targets of IFN-I production (left) and signaling (right) are indicated. Viral proteins with IFN-I inhibitory activities but with unknown targets are indicated in red boxes and question marks. See text for details. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; IFN-I, type I interferon.
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