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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 Science 2020 ; 369 (6508): 1210-1220 Nephropedia Template TP
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Systems biological assessment of immunity to mild versus severe COVID-19 infection in humans #MMPMID32788292
Arunachalam PS; Wimmers F; Mok CKP; Perera RAPM; Scott M; Hagan T; Sigal N; Feng Y; Bristow L; Tak-Yin Tsang O; Wagh D; Coller J; Pellegrini KL; Kazmin D; Alaaeddine G; Leung WS; Chan JMC; Chik TSH; Choi CYC; Huerta C; Paine McCullough M; Lv H; Anderson E; Edupuganti S; Upadhyay AA; Bosinger SE; Maecker HT; Khatri P; Rouphael N; Peiris M; Pulendran B
Science 2020[Sep]; 369 (6508): 1210-1220 PMID32788292show ga
Coronavirus disease 2019 (COVID-19) represents a global crisis, yet major knowledge gaps remain about human immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We analyzed immune responses in 76 COVID-19 patients and 69 healthy individuals from Hong Kong and Atlanta, Georgia, United States. In the peripheral blood mononuclear cells (PBMCs) of COVID-19 patients, we observed reduced expression of human leukocyte antigen class DR (HLA-DR) and proinflammatory cytokines by myeloid cells as well as impaired mammalian target of rapamycin (mTOR) signaling and interferon-alpha (IFN-alpha) production by plasmacytoid dendritic cells. By contrast, we detected enhanced plasma levels of inflammatory mediators-including EN-RAGE, TNFSF14, and oncostatin M-which correlated with disease severity and increased bacterial products in plasma. Single-cell transcriptomics revealed a lack of type I IFNs, reduced HLA-DR in the myeloid cells of patients with severe COVID-19, and transient expression of IFN-stimulated genes. This was consistent with bulk PBMC transcriptomics and transient, low IFN-alpha levels in plasma during infection. These results reveal mechanisms and potential therapeutic targets for COVID-19.