L. Kuri-Cervantes, M. B. Pampena, W. Meng, Aaron M. Rosenfeld, C. Ittner, A. Weisman, R. Agyekum, D. Mathew, A. Baxter, L. Vella, O. Kuthuru, S. Apostolidis, Luanne Bershaw, J. Dougherty, A. Greenplate, A. Pattekar, Justin Kim, N. Han, S. Gouma, M. Weirick, C. P. Arevalo, M. Bolton, E. Goodwin, E. M. Anderson, S. Hensley, T. Jones, N. Mangalmurti, E. L. Luning Prak, E. Wherry, N. Meyer, M. Betts
Science Immunology, 2020
Although critical illness has been associated with SARS-CoV-2-induced hyperinflammation, the immune correlates of severe COVID-19 remain unclear. Here, we comprehensively analyzed peripheral blood immune perturbations in 42 SARS-CoV-2 infected and recovered individuals. We identified extensive induction and activation of multiple immune lineages, including T cell activation, oligoclonal plasmablast expansion, and Fc and trafficking receptor modulation on innate lymphocytes and granulocytes, that distinguished severe COVID-19 cases from healthy donors or SARS-CoV-2-recovered or moderate severity patients. We found the neutrophil to lymphocyte ratio to be a prognostic biomarker of disease severity and organ failure. Our findings demonstrate broad innate and adaptive leukocyte perturbations that distinguish dysregulated host responses in severe SARS-CoV-2 infection and warrant therapeutic investigation. Profound plasmablast expansion, innate cell modulation, and T cell activation are defining features of severe COVID-19.
Cited by 242 publications.
Field of study: Medicine