Immune phenotypes that are associated with subsequent COVID-19 severity inferred from post-recovery samples

Thomas Liechti (), Yaser Iftikhar, Massimo Mangino, Margaret Beddall, Charles W. Goss, Jane A. O’Halloran, Philip A. Mudd and Mario Roederer ()
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Thomas Liechti: ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH
Yaser Iftikhar: ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH
Massimo Mangino: King’s College of London
Margaret Beddall: ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH
Charles W. Goss: Washington University School of Medicine
Jane A. O’Halloran: Washington University School of Medicine
Philip A. Mudd: Washington University School of Medicine
Mario Roederer: ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Severe COVID-19 causes profound immune perturbations, but pre-infection immune signatures contributing to severe COVID-19 remain unknown. Genome-wide association studies (GWAS) identified strong associations between severe disease and several chemokine receptors and molecules from the type I interferon pathway. Here, we define immune signatures associated with severe COVID-19 using high-dimensional flow cytometry. We measure the cells of the peripheral immune system from individuals who recovered from mild, moderate, severe or critical COVID-19 and focused only on those immune signatures returning to steady-state. Individuals that suffered from severe COVID-19 show reduced frequencies of T cell, mucosal-associated invariant T cell (MAIT) and dendritic cell (DC) subsets and altered chemokine receptor expression on several subsets, such as reduced levels of CCR1 and CCR2 on monocyte subsets. Furthermore, we find reduced frequencies of type I interferon-producing plasmacytoid DCs and altered IFNAR2 expression on several myeloid cells in individuals recovered from severe COVID-19. Thus, these data identify potential immune mechanisms contributing to severe COVID-19.

Date: 2022
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DOI: 10.1038/s41467-022-34638-2

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