Immunological imprint of COVID‐19 on human peripheral blood leukocyte populations

gnorimies2015 shared this article with you from Inoreader Immunological imprint of COVID‐19 on human peripheral blood leukocyte populations Via Allergy Abstract Background SARS‐CoV‐2 has triggered a pandemic that is now claiming many lives. Several studies have investigated cellular immune responses in COVID‐19 patients during disease but little is known regarding a possible protracted impact of COVID‐19 on the adaptive and innate immune system in COVID‐19‐convalescent patients. Methods We used multiparametric flow cytometry to analyze whole peripheral blood samples, and determined SARS‐CoV‐2 specific antibody levels against the S‐protein, its RBD‐subunit and viral nucleocapsid in a cohort of COVID‐19 convalescent patients who had mild disease approximately 10 weeks after infection (n=109) and healthy control subjects (n=98). Furthermore, we correlated immunological changes with clinical and demographic parameters. Results Even ten weeks after disease COVID‐19 convalescent patients had fewer neutrophils, while their cytotoxic CD8+ T cells were activated, reflected as higher HLA‐DR and CD38 expression. Multiparametric regression analyses showed that in COVID‐19 patients both CD3+CD4+ and CD3+CD8+ effector memory cells were higher, while CD25+Foxp3+ T regulatory cells were lower. In addition, both transitional B cell and plasmablast levels were significantly elevated in COVID‐19 patients. Fever (duration, level) correlated with numbers of central memory CD4+ T cells and anti‐S and anti‐RBD, but not anti‐NC antibody levels. Moreover, a "young immunological age" as determined by numbers of CD3+CD45RA+CD62L+CD31+ recent thymic emigrants was associated with a loss of sense of taste and/or smell. Conclusion Acute SARS‐CoV‐2 infection leaves protracted beneficial (i.e., activation of T cells) and potentially harmful (i.e., reduction of neutrophils) imprints in the cellular immune system in addition to induction of specific antibody responses. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.