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

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...

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Detalles Bibliográficos
Autores principales: Xia, Hongjie, Shi, Pei-Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mary Ann Liebert, Inc., publishers 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757701/
https://www.ncbi.nlm.nih.gov/pubmed/33337934
http://dx.doi.org/10.1089/jir.2020.0214
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author Xia, Hongjie
Shi, Pei-Yong
author_facet Xia, Hongjie
Shi, Pei-Yong
author_sort Xia, Hongjie
collection PubMed
description 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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spelling pubmed-77577012020-12-28 Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2 Xia, Hongjie Shi, Pei-Yong J Interferon Cytokine Res Reviews 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. Mary Ann Liebert, Inc., publishers 2020-12-01 2020-12-16 /pmc/articles/PMC7757701/ /pubmed/33337934 http://dx.doi.org/10.1089/jir.2020.0214 Text en © Hongjie Xia and Pei-Yong Shi 2020; Published by Mary Ann Liebert, Inc. This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are cited.
spellingShingle Reviews
Xia, Hongjie
Shi, Pei-Yong
Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title_full Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title_fullStr Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title_full_unstemmed Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title_short Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2
title_sort antagonism of type i interferon by severe acute respiratory syndrome coronavirus 2
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757701/
https://www.ncbi.nlm.nih.gov/pubmed/33337934
http://dx.doi.org/10.1089/jir.2020.0214
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