DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, You-Me | ko |
dc.contributor.author | Shin, Eui-Cheol | ko |
dc.date.accessioned | 2021-06-22T01:31:12Z | - |
dc.date.available | 2021-06-22T01:31:12Z | - |
dc.date.created | 2021-06-01 | - |
dc.date.created | 2021-06-01 | - |
dc.date.created | 2021-06-01 | - |
dc.date.issued | 2021-05 | - |
dc.identifier.citation | EXPERIMENTAL AND MOLECULAR MEDICINE, v.53, no.5, pp.750 - 760 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.uri | http://hdl.handle.net/10203/286078 | - |
dc.description.abstract | SARS-CoV-2: exploring virus-triggered immune system dysfunction Extensive studies into how SARS-CoV-2 manipulates the immune system and influences the activity of host proteins are needed to improve treatments for COVID-19. SARS-CoV-2 evades or blocks elements of the immune system, including the antiviral activity of type I and type III interferons (IFN). You-Me Kim and Eui-Cheol Shin at the Korea Advanced Institute of Science and Technology, Daejeon, South Korea, reviewed understanding of how SARS-CoV-2 inhibits IFN responses. In infected cells, SARS-CoV-2 proteins use diverse methods to inhibit host IFN pathways, but type I IFN responses are still triggered in non-infected immune cells. The researchers believe this may explain the delayed but exaggerated type I IFN responses that contribute to the hyper-inflammation seen in critically ill patients. They call for further investigations into IFN and inflammatory responses in SARS-CoV-2 infection. Coronavirus disease 2019 (COVID-19), the current pandemic disease, is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Type I and III interferons (IFNs) are innate cytokines that are important in the first-line defense against viruses. Similar to many other viruses, SARS-CoV-2 has evolved mechanisms for evading the antiviral effects of type I and III IFNs at multiple levels, including the induction of IFN expression and cellular responses to IFNs. In this review, we describe the innate sensing mechanisms of SARS-CoV-2 and the mechanisms used by SARS-CoV-2 to evade type I and III IFN responses. We also discuss contradictory reports regarding impaired and robust type I IFN responses in patients with severe COVID-19. Finally, we discuss how delayed but exaggerated type I IFN responses can exacerbate inflammation and contribute to the severe progression of COVID-19. | - |
dc.language | English | - |
dc.publisher | SPRINGERNATURE | - |
dc.title | Type I and III interferon responses in SARS-CoV-2 infection | - |
dc.type | Article | - |
dc.identifier.wosid | 000647530800005 | - |
dc.identifier.scopusid | 2-s2.0-85105261706 | - |
dc.type.rims | ART | - |
dc.citation.volume | 53 | - |
dc.citation.issue | 5 | - |
dc.citation.beginningpage | 750 | - |
dc.citation.endingpage | 760 | - |
dc.citation.publicationname | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.identifier.doi | 10.1038/s12276-021-00592-0 | - |
dc.identifier.kciid | ART002714655 | - |
dc.contributor.localauthor | Kim, You-Me | - |
dc.contributor.localauthor | Shin, Eui-Cheol | - |
dc.description.isOpenAccess | Y | - |
dc.type.journalArticle | Review | - |
dc.subject.keywordPlus | INNATE IMMUNITY | - |
dc.subject.keywordPlus | CORONAVIRUS | - |
dc.subject.keywordPlus | ANTAGONISM | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | DISTINCT | - |
dc.subject.keywordPlus | EVASION | - |
dc.subject.keywordPlus | DOMAIN | - |
dc.subject.keywordPlus | STAT1 | - |
dc.subject.keywordPlus | NSP1 | - |
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