4.2 Review

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

Journal

JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
Volume 40, Issue 12, Pages 543-548

Publisher

MARY ANN LIEBERT, INC
DOI: 10.1089/jir.2020.0214

Keywords

SARS-CoV-2; COVID-19; interferon; immune evasion

Funding

  1. NIH [AI142759, AI134907, AI145617, UL1TR001439]
  2. Sealy & Smith Foundation
  3. John S. Dunn Foundation
  4. Amon G. Carter Foundation
  5. Gillson Longenbaugh Foundation
  6. Summerfield Robert Foundation
  7. Kleberg Foundation

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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.

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