Abstract:
SARS-CoV-2 causes a spectrum of illness, ranging from asymptomatic to severe COVID-19. Early in March when WHO declared the COVID-19 pandemic, we provided the first evidence that the breadth of robust immune responses to SARS-CoV2 can be measured in peripheral blood prior to patient recovery. This was a longitudinal case study of one patient. As the immunological basis for severity remains ill-defined, we have now analysed 78 SARS-CoV-2-infected individuals at acute and/or convalescent timepoints, up to 102 days post-symptom onset, quantifying 184 innate and adaptive immunological parameters. Acute hospitalised COVID-19, including ward and intensive care unit (ICU) patients, was associated with high levels of IL-6, IL-18 and IL-10, elevated neutrophil-to-lymphocyte and neutrophil-to-T cell ratios, and high proportions of activated CD38+ neutrophils, CD38+ eosinophils, CD38+HLA-DRlo monocytes, CD38+CD56dim NK cells, CD38+ γδ T cells, antibody-secreting cells, PD-1+ICOS+ circulating T follicular helper (cTFH) cells, CD38+HLA-DR+CD4+ T cells, effector CD27-CD45RA+ and CD38+CD8+ T cells. During convalescence, elevated seroconversion and neutralising antibodies were prominent and correlated with acute CXCR3+ cTFH cell activation. Strikingly, ICU patients with severe COVID-19 displayed higher levels of soluble IL-6R, IL-18, and hyperactivation of innate, adaptive and myeloid compartments than ward patients with moderate disease. Our analyses provide a comprehensive map of longitudinal immunological responses in COVID-19 patients during acute and convalescent phases of SARS-CoV-2 infection, and integrate key cellular pathways of complex perturbed immune networks that underpin severe COVID-19. We observed a typical immune response in people displaying mild to moderate infections and that this immune response was not controlled in time in patients suffering from severe disease. Our data also provides important insights into potential biomarkers and immunotherapies for severer cases such as higher IL-18, IL-6R, IL-6 and CD38 expression on innate and adaptive immune cells.