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10.1038/s12276-021-00592-0

http://scihub22266oqcxt.onion/10.1038/s12276-021-00592-0
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33953323!8099704!33953323
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suck abstract from ncbi


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pmid33953323      Exp+Mol+Med 2021 ; 53 (5): 750-760
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  • Type I and III interferon responses in SARS-CoV-2 infection #MMPMID33953323
  • Kim YM; Shin EC
  • Exp Mol Med 2021[May]; 53 (5): 750-760 PMID33953323show ga
  • 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.
  • |*Immune Evasion[MESH]
  • |*Immunity, Innate[MESH]
  • |Animals[MESH]
  • |COVID-19/genetics/*immunology[MESH]
  • |Gene Expression Regulation[MESH]
  • |Humans[MESH]
  • |Inflammation/genetics/immunology[MESH]
  • |Interferon Lambda[MESH]
  • |Interferon Type I/genetics/*immunology[MESH]
  • |Interferons/genetics/*immunology[MESH]


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