The type I interferon response in COVID-19: implications for treatment
Despite early reports to the contrary, there is increasing evidence that patients with severe COVID-19 have a robust type I interferon response, which contrasts with the delayed, possibly suppressed, interferon response seen early in infection. A robust type I interferon response could exacerbate hy...
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Veröffentlicht in: | Nature reviews. Immunology 2020-10, Vol.20 (10), p.585-586 |
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description | Despite early reports to the contrary, there is increasing evidence that patients with severe COVID-19 have a robust type I interferon response, which contrasts with the delayed, possibly suppressed, interferon response seen early in infection. A robust type I interferon response could exacerbate hyperinflammation in the progression to severe COVID-19 through diverse mechanisms. Further understanding of the roles of type I interferon at different stages of infection and in patients with mild versus severe COVID-19 will provide insights for the therapeutic use of interferon administration or JAK inhibitors in patients with COVID-19.
In this Comment, Jeong Seok Lee and Eui-Cheol Shin discuss contradictory results regarding the downregulation or upregulation of type I interferon responses in patients with COVID-19 and the implications for therapies that target this pathway. |
doi_str_mv | 10.1038/s41577-020-00429-3 |
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therapeutic use</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jeong Seok</creatorcontrib><creatorcontrib>Shin, Eui-Cheol</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature reviews. Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jeong Seok</au><au>Shin, Eui-Cheol</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The type I interferon response in COVID-19: implications for treatment</atitle><jtitle>Nature reviews. Immunology</jtitle><stitle>Nat Rev Immunol</stitle><addtitle>Nat Rev Immunol</addtitle><date>2020-10-01</date><risdate>2020</risdate><volume>20</volume><issue>10</issue><spage>585</spage><epage>586</epage><pages>585-586</pages><issn>1474-1733</issn><eissn>1474-1741</eissn><abstract>Despite early reports to the contrary, there is increasing evidence that patients with severe COVID-19 have a robust type I interferon response, which contrasts with the delayed, possibly suppressed, interferon response seen early in infection. A robust type I interferon response could exacerbate hyperinflammation in the progression to severe COVID-19 through diverse mechanisms. Further understanding of the roles of type I interferon at different stages of infection and in patients with mild versus severe COVID-19 will provide insights for the therapeutic use of interferon administration or JAK inhibitors in patients with COVID-19.
In this Comment, Jeong Seok Lee and Eui-Cheol Shin discuss contradictory results regarding the downregulation or upregulation of type I interferon responses in patients with COVID-19 and the implications for therapies that target this pathway.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32788708</pmid><doi>10.1038/s41577-020-00429-3</doi><tpages>2</tpages><orcidid>https://orcid.org/0000-0002-6308-9503</orcidid><orcidid>https://orcid.org/0000-0001-8261-7044</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 631/250/127/1212 692/699/255/2514 Azetidines - therapeutic use Betacoronavirus - immunology Betacoronavirus - pathogenicity Biological response modifiers Biomedical and Life Sciences Biomedicine Comment Coronavirus Infections - drug therapy Coronavirus Infections - immunology Coronavirus Infections - pathology Coronavirus Infections - virology Coronaviruses COVID-19 Gene Expression Regulation Health aspects Humans Immunity, Cellular - drug effects Immunity, Humoral - drug effects Immunology Infection Interferon Interferon Regulatory Factors - genetics Interferon Regulatory Factors - immunology Interferon-alpha - genetics Interferon-alpha - immunology Interferon-alpha - therapeutic use Interferon-beta - genetics Interferon-beta - immunology Interferon-beta - therapeutic use Interferons - genetics Interferons - immunology Interferons - therapeutic use Interleukin-1 - genetics Interleukin-1 - immunology Interleukin-6 - antagonists & inhibitors Interleukin-6 - genetics Interleukin-6 - immunology Janus Kinase 1 - antagonists & inhibitors Janus Kinase 1 - genetics Janus Kinase 1 - immunology Lung - drug effects Lung - immunology Lung - pathology Pandemics Pneumonia, Viral - drug therapy Pneumonia, Viral - immunology Pneumonia, Viral - pathology Pneumonia, Viral - virology Purines Pyrazoles SARS-CoV-2 Severity of Illness Index Sulfonamides - therapeutic use Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology |
title | The type I interferon response in COVID-19: implications for treatment |
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