The Journal of infectious diseases
Authors: Lagenaur LA, Hemmerling A, Chiu C, Miller S, Lee PP, Cohen CR, Parks TP
Environmental health perspectives
Authors: Murphy MB, Huang AS, Schick SF
Hepatology communications
Authors: Patel AA, Woodrell C, Ufere NN, Hansen L, Tandon P, Verma M, Lai J, Pinotti R, Rakoski M, Palliative Care Education, Advocacy, and Research in Liver Disease (PEARL) Workgroup and the AASLD P
The American journal of medicine
Authors: Onumah CM, Lai CJ, Levine D, Ismail N, Pincavage AT, Osman NY
The Lancet. Infectious diseases
Authors: Andolina C, Rek JC, Briggs J, Okoth J, Musiime A, Ramjith J, Teyssier N, Conrad M, Nankabirwa JI, Lanke K, Rodriguez-Barraquer I, Meerstein-Kessel L, Arinaitwe E, Olwoch P, Rosenthal PJ, Kamya MR, Dorsey G, Greenhouse B, Drakeley C, Staedke SG, Bousema T
FASEB bioAdvances
Authors: Chen CL, Huang FW, Huang SS, Huang JS
Digestive diseases and sciences
Authors: Ha NB, Cho SJ, Mohamad Y, Kent D, Jun G, Wong R, Swarnakar V, Lin S, Maher JJ, Lai JC
Volume 218 of Issue 8 | The Journal of experimental medicine
Authors: Wilk AJ, Lee MJ, Wei B, Parks B, Pi R, Martínez-Colón GJ, Ranganath T, Zhao NQ, Taylor S, Becker W, Stanford COVID-19 Biobank, Jimenez-Morales D, Blomkalns AL, O'Hara R, Ashley EA, Nadeau KC, Yang S, Holmes S, Rabinovitch M, Rogers AJ, Greenleaf WJ, Blish CA
Our understanding of protective versus pathological immune responses to SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19), is limited by inadequate profiling of patients at the extremes of the disease severity spectrum. Here, we performed multi-omic single-cell immune profiling of 64 COVID-19 patients across the full range of disease severity, from outpatients with mild disease to fatal cases. Our transcriptomic, epigenomic, and proteomic analyses revealed widespread dysfunction of peripheral innate immunity in severe and fatal COVID-19, including prominent hyperactivation signatures in neutrophils and NK cells. We also identified chromatin accessibility changes at NF-κB binding sites within cytokine gene loci as a potential mechanism for the striking lack of pro-inflammatory cytokine production observed in monocytes in severe and fatal COVID-19. We further demonstrated that emergency myelopoiesis is a prominent feature of fatal COVID-19. Collectively, our results reveal disease severity-associated immune phenotypes in COVID-19 and identify pathogenesis-associated pathways that are potential targets for therapeutic intervention.
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JACC. CardioOncology
Authors: Schlam I, Lee AY, Li S, Sheikh FH, Zaghlol R, Basyal B, Gallagher C, Molina E, Mahr C, Cheng RK, Barac A
Heart (British Cardiac Society)
Authors: Leedy D, Tiwana JK, Mamas M, Hira R, Cheng R
