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10.1016/j.cell.2020.04.035

http://scihub22266oqcxt.onion/10.1016/j.cell.2020.04.035
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32413319!7252096!32413319
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suck abstract from ncbi


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pmid32413319      Cell 2020 ; 181 (5): 1016-1035.e19
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  • SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues #MMPMID32413319
  • Ziegler CGK; Allon SJ; Nyquist SK; Mbano IM; Miao VN; Tzouanas CN; Cao Y; Yousif AS; Bals J; Hauser BM; Feldman J; Muus C; Wadsworth MH 2nd; Kazer SW; Hughes TK; Doran B; Gatter GJ; Vukovic M; Taliaferro F; Mead BE; Guo Z; Wang JP; Gras D; Plaisant M; Ansari M; Angelidis I; Adler H; Sucre JMS; Taylor CJ; Lin B; Waghray A; Mitsialis V; Dwyer DF; Buchheit KM; Boyce JA; Barrett NA; Laidlaw TM; Carroll SL; Colonna L; Tkachev V; Peterson CW; Yu A; Zheng HB; Gideon HP; Winchell CG; Lin PL; Bingle CD; Snapper SB; Kropski JA; Theis FJ; Schiller HB; Zaragosi LE; Barbry P; Leslie A; Kiem HP; Flynn JL; Fortune SM; Berger B; Finberg RW; Kean LS; Garber M; Schmidt AG; Lingwood D; Shalek AK; Ordovas-Montanes J
  • Cell 2020[May]; 181 (5): 1016-1035.e19 PMID32413319show ga
  • There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.
  • |Adolescent[MESH]
  • |Alveolar Epithelial Cells/immunology/*metabolism[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Animals[MESH]
  • |Betacoronavirus/physiology[MESH]
  • |COVID-19[MESH]
  • |Cell Line[MESH]
  • |Cells, Cultured[MESH]
  • |Child[MESH]
  • |Coronavirus Infections/virology[MESH]
  • |Enterocytes/immunology/*metabolism[MESH]
  • |Goblet Cells/immunology/*metabolism[MESH]
  • |HIV Infections/immunology[MESH]
  • |Humans[MESH]
  • |Influenza, Human/immunology[MESH]
  • |Interferon Type I/immunology/*metabolism[MESH]
  • |Lung/cytology/pathology[MESH]
  • |Macaca mulatta[MESH]
  • |Mice[MESH]
  • |Mycobacterium tuberculosis[MESH]
  • |Nasal Mucosa/*cytology/immunology[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/*genetics/metabolism[MESH]
  • |Pneumonia, Viral/virology[MESH]
  • |Receptors, Virus/genetics[MESH]
  • |SARS-CoV-2[MESH]
  • |Serine Endopeptidases/metabolism[MESH]
  • |Single-Cell Analysis[MESH]
  • |Tuberculosis/immunology[MESH]


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