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Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for thi...

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Detalles Bibliográficos
Autores principales: King, Cecile, Sprent, Jonathan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879020/
https://www.ncbi.nlm.nih.gov/pubmed/33622601
http://dx.doi.org/10.1016/j.it.2021.02.003
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author King, Cecile
Sprent, Jonathan
author_facet King, Cecile
Sprent, Jonathan
author_sort King, Cecile
collection PubMed
description Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design.
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spelling pubmed-78790202021-02-16 Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation King, Cecile Sprent, Jonathan Trends Immunol Review Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design. Elsevier Ltd. 2021-04 2021-02-12 /pmc/articles/PMC7879020/ /pubmed/33622601 http://dx.doi.org/10.1016/j.it.2021.02.003 Text en © 2021 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Review
King, Cecile
Sprent, Jonathan
Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title_full Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title_fullStr Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title_full_unstemmed Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title_short Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation
title_sort dual nature of type i interferons in sars-cov-2-induced inflammation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879020/
https://www.ncbi.nlm.nih.gov/pubmed/33622601
http://dx.doi.org/10.1016/j.it.2021.02.003
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