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COVID‐19: lambda interferon against viral load and hyperinflammation
Coronavirus disease 2019 (COVID‐19), triggered by the betacoronavirus SARS‐CoV‐2, has become one of the worst pandemics of our time that has already caused more than 250,000 deaths (JHU data‐05/06/2020, https://coronavirus.jhu.edu/). Effective therapeutic approaches are urgently needed to reduce the...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267110/ https://www.ncbi.nlm.nih.gov/pubmed/32333818 http://dx.doi.org/10.15252/emmm.202012465 |
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author | Andreakos, Evangelos Tsiodras, Sotirios |
author_facet | Andreakos, Evangelos Tsiodras, Sotirios |
author_sort | Andreakos, Evangelos |
collection | PubMed |
description | Coronavirus disease 2019 (COVID‐19), triggered by the betacoronavirus SARS‐CoV‐2, has become one of the worst pandemics of our time that has already caused more than 250,000 deaths (JHU data‐05/06/2020, https://coronavirus.jhu.edu/). Effective therapeutic approaches are urgently needed to reduce the spread of the virus and its death toll. Here, we assess the possibility of using interferon‐lambda (IFNλ), a third type of interferon sharing low homology with type I IFNs and IL‐10, for treating COVID‐19 patients. We discuss the unique role of IFNλ in fine‐tuning antiviral immunity in the respiratory tract to achieve optimal protection and minimal host damage and review early evidence that SARS‐CoV‐2 may impair IFNλ induction, leading to a delayed type I IFN‐dominated response that triggers hyperinflammation and severe disease. We also consider the potential windows of opportunity for therapeutic intervention with IFNλ and potential safety considerations. We conclude that IFNλ constitutes a promising therapeutic agent for reducing viral presence and hyperinflammation in a single shot to prevent the devastating consequences of COVID‐19 such as pneumonia and acute respiratory distress syndrome (ARDS). |
format | Online Article Text |
id | pubmed-7267110 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-72671102020-06-03 COVID‐19: lambda interferon against viral load and hyperinflammation Andreakos, Evangelos Tsiodras, Sotirios EMBO Mol Med Commentaries Coronavirus disease 2019 (COVID‐19), triggered by the betacoronavirus SARS‐CoV‐2, has become one of the worst pandemics of our time that has already caused more than 250,000 deaths (JHU data‐05/06/2020, https://coronavirus.jhu.edu/). Effective therapeutic approaches are urgently needed to reduce the spread of the virus and its death toll. Here, we assess the possibility of using interferon‐lambda (IFNλ), a third type of interferon sharing low homology with type I IFNs and IL‐10, for treating COVID‐19 patients. We discuss the unique role of IFNλ in fine‐tuning antiviral immunity in the respiratory tract to achieve optimal protection and minimal host damage and review early evidence that SARS‐CoV‐2 may impair IFNλ induction, leading to a delayed type I IFN‐dominated response that triggers hyperinflammation and severe disease. We also consider the potential windows of opportunity for therapeutic intervention with IFNλ and potential safety considerations. We conclude that IFNλ constitutes a promising therapeutic agent for reducing viral presence and hyperinflammation in a single shot to prevent the devastating consequences of COVID‐19 such as pneumonia and acute respiratory distress syndrome (ARDS). John Wiley and Sons Inc. 2020-05-25 2020-06-08 /pmc/articles/PMC7267110/ /pubmed/32333818 http://dx.doi.org/10.15252/emmm.202012465 Text en © 2020 The Authors. Published under the terms of the CC BY 4.0 license This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Commentaries Andreakos, Evangelos Tsiodras, Sotirios COVID‐19: lambda interferon against viral load and hyperinflammation |
title |
COVID‐19: lambda interferon against viral load and hyperinflammation |
title_full |
COVID‐19: lambda interferon against viral load and hyperinflammation |
title_fullStr |
COVID‐19: lambda interferon against viral load and hyperinflammation |
title_full_unstemmed |
COVID‐19: lambda interferon against viral load and hyperinflammation |
title_short |
COVID‐19: lambda interferon against viral load and hyperinflammation |
title_sort | covid‐19: lambda interferon against viral load and hyperinflammation |
topic | Commentaries |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267110/ https://www.ncbi.nlm.nih.gov/pubmed/32333818 http://dx.doi.org/10.15252/emmm.202012465 |
work_keys_str_mv | AT andreakosevangelos covid19lambdainterferonagainstviralloadandhyperinflammation AT tsiodrassotirios covid19lambdainterferonagainstviralloadandhyperinflammation |