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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...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mary Ann Liebert, Inc., publishers
2020
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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. |
format | Online Article Text |
id | pubmed-7757701 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Mary Ann Liebert, Inc., publishers |
record_format | MEDLINE/PubMed |
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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