Journal
CELL REPORTS MEDICINE
Volume 2, Issue 5, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.xcrm.2021.100287
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Funding
- Cystic Fibrosis Foundation Postdoctoral Fellowship [LIN19F0]
- NIH/NIAID [U19 AI082630]
- Harvard Catalyst/Harvard Clinical and Translational Science Center (National Center for Advancing Translational Sciences, National Institutes of Health) [UL1 TR 001102, UL1 TR 002541-01]
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This study analyzed thousands of plasma proteins longitudinally in COVID-19 patients, uncovering immune and non-immune proteins linked to the disease. Dynamic immune-cell-derived and tissue-associated proteins associated with survival were identified. The research proposed a model in which interactions among myeloid, epithelial, and T cells drive tissue damage in severe COVID-19 disease.
Mechanisms underlying severe coronavirus disease 2019 (COVID-19) disease remain poorly understood. We analyze several thousand plasma proteins longitudinally in 306 COVID-19 patients and 78 symptomatic controls, uncovering immune and non-immune proteins linked to COVID-19. Deconvolution of our plasma proteome data using published scRNA-seq datasets reveals contributions from circulating immune and tissue cells. Sixteen percent of patients display reduced inflammation yet comparably poor outcomes. Comparison of patients who died to severely ill survivors identifies dynamic immune-cell-derived and tissue-associated proteins associated with survival, including exocrine pancreatic proteases. Using derived tissue-specific and cell-type-specific intracellular death signatures, cellular angiotensin-converting enzyme 2 (ACE2) expression, and our data, we infer whether organ damage resulted from direct or indirect effects of infection. We propose a model in which interactions among myeloid, epithelial, and T cells drive tissue damage. These datasets provide important insights and a rich resource for analysis of mechanisms of severe COVID-19 disease.
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