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10.1016/j.isci.2021.102477

http://scihub22266oqcxt.onion/10.1016/j.isci.2021.102477
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suck abstract from ncbi


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pmid33937724      iScience 2021 ; 24 (5): 102477
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  • Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses #MMPMID33937724
  • Banerjee A; El-Sayes N; Budylowski P; Jacob RA; Richard D; Maan H; Aguiar JA; Demian WL; Baid K; D'Agostino MR; Ang JC; Murdza T; Tremblay BJ; Afkhami S; Karimzadeh M; Irving AT; Yip L; Ostrowski M; Hirota JA; Kozak R; Capellini TD; Miller MS; Wang B; Mubareka S; McGeer AJ; McArthur AG; Doxey AC; Mossman K
  • iScience 2021[May]; 24 (5): 102477 PMID33937724show ga
  • Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNalpha detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.
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