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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell 2021 ; 184 (18): 4713-4733.e22 Nephropedia Template TP
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Impaired local intrinsic immunity to SARS-CoV-2 infection in severe COVID-19 #MMPMID34352228
Ziegler CGK; Miao VN; Owings AH; Navia AW; Tang Y; Bromley JD; Lotfy P; Sloan M; Laird H; Williams HB; George M; Drake RS; Christian T; Parker A; Sindel CB; Burger MW; Pride Y; Hasan M; Abraham GE 3rd; Senitko M; Robinson TO; Shalek AK; Glover SC; Horwitz BH; Ordovas-Montanes J
Cell 2021[Sep]; 184 (18): 4713-4733.e22 PMID34352228show ga
SARS-CoV-2 infection can cause severe respiratory COVID-19. However, many individuals present with isolated upper respiratory symptoms, suggesting potential to constrain viral pathology to the nasopharynx. Which cells SARS-CoV-2 primarily targets and how infection influences the respiratory epithelium remains incompletely understood. We performed scRNA-seq on nasopharyngeal swabs from 58 healthy and COVID-19 participants. During COVID-19, we observe expansion of secretory, loss of ciliated, and epithelial cell repopulation via deuterosomal cell expansion. In mild and moderate COVID-19, epithelial cells express anti-viral/interferon-responsive genes, while cells in severe COVID-19 have muted anti-viral responses despite equivalent viral loads. SARS-CoV-2 RNA(+) host-target cells are highly heterogenous, including developing ciliated, interferon-responsive ciliated, AZGP1(high) goblet, and KRT13(+) "hillock"-like cells, and we identify genes associated with susceptibility, resistance, or infection response. Our study defines protective and detrimental responses to SARS-CoV-2, the direct viral targets of infection, and suggests that failed nasal epithelial anti-viral immunity may underlie and precede severe COVID-19.