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10.1101/2020.04.09.034454

http://scihub22266oqcxt.onion/10.1101/2020.04.09.034454
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32511326!7239056!32511326
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suck abstract from ncbi


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pmid32511326      bioRxiv 2020 ; ä (ä): ä
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  • Type 2 and interferon inflammation strongly regulate SARS-CoV-2 related gene expression in the airway epithelium #MMPMID32511326
  • Sajuthi SP; DeFord P; Jackson ND; Montgomery MT; Everman JL; Rios CL; Pruesse E; Nolin JD; Plender EG; Wechsler ME; Mak AC; Eng C; Salazar S; Medina V; Wohlford EM; Huntsman S; Nickerson DA; Germer S; Zody MC; Abecasis G; Kang HM; Rice KM; Kumar R; Oh S; Rodriguez-Santana J; Burchard EG; Seibold MA
  • bioRxiv 2020[Apr]; ä (ä): ä PMID32511326show ga
  • Coronavirus disease 2019 (COVID-19) outcomes vary from asymptomatic infection to death. This disparity may reflect different airway levels of the SARS-CoV-2 receptor, ACE2, and the spike protein activator, TMPRSS2. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci (eQTL) for both ACE2 and TMPRSS2, that vary in frequency across world populations. Importantly, we find TMPRSS2 is part of a mucus secretory network, highly upregulated by T2 inflammation through the action of interleukin-13, and that interferon response to respiratory viruses highly upregulates ACE2 expression. Finally, we define airway responses to coronavirus infections in children, finding that these infections upregulate IL6 while also stimulating a more pronounced cytotoxic immune response relative to other respiratory viruses. Our results reveal mechanisms likely influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes.
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