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

Hongjie Xia; Pei Yong Shi

doi:10.1089/jir.2020.0214

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

Hongjie Xia, Pei Yong Shi

Biochemistry & Molecular Biology

Research output: Contribution to journal › Review article › peer-review

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.

Original language	English (US)
Pages (from-to)	543-548
Number of pages	6
Journal	Journal of Interferon and Cytokine Research
Volume	40
Issue number	12
DOIs	https://doi.org/10.1089/jir.2020.0214
State	Published - Dec 2020

Keywords

COVID-19
SARS-CoV-2
immune evasion
interferon

ASJC Scopus subject areas

Immunology
Cell Biology
Virology

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10.1089/jir.2020.0214

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COVID-19 virus helps block host immunity
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title = "Antagonism of Type i Interferon by Severe Acute Respiratory Syndrome Coronavirus 2",

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",

author = "Hongjie Xia and Shi, {Pei Yong}",

note = "Funding Information: P.-Y.S. was supported by NIH grants AI142759, AI134907, AI145617, and UL1TR001439, and awards from the Sealy & Smith Foundation, Kleberg Foundation, the John S. Dunn Foundation, the Amon G. Carter Foundation, the Gillson Longenbaugh Foundation, and the Summerfield Robert Foundation.",

year = "2020",

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doi = "10.1089/jir.2020.0214",

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N2 - 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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Antagonism of Type i Interferon by Severe Acute Respiratory Syndrome Coronavirus 2

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

COVID-19 virus helps block host immunity

Cite this