Evolution of immune responses to SARS-CoV-2 in mild-moderate COVID-19

Adam K. Wheatley(Australian Research Council), Jennifer A. Juno(The University of Melbourne), Jing Jing Wang(Flinders University), Kevin J. Selva(The University of Melbourne), Arnold Reynaldi(UNSW Sydney), Hyon‐Xhi Tan(The University of Melbourne), Wen Shi Lee(The University of Melbourne), Kathleen M. Wragg(The University of Melbourne), Hannah G. Kelly(Australian Research Council), Robyn Esterbauer(Australian Research Council), Samantha K. Davis(The University of Melbourne), Helen E. Kent(The University of Melbourne), Francesca L. Mordant(The University of Melbourne), Timothy E. Schlub(The University of Sydney), David Gordon(South Australia Pathology), David S. Khoury(UNSW Sydney), Kanta Subbarao(The University of Melbourne), Deborah Cromer(UNSW Sydney), Tom P. Gordon(South Australia Pathology), Amy W. Chung(The University of Melbourne), Miles P. Davenport(UNSW Sydney), Stephen J. Kent(Australian Research Council)
Nature Communications
February 19, 2021
Cited by 410Open Access
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Abstract

Abstract The durability of infection-induced SARS-CoV-2 immunity has major implications for reinfection and vaccine development. Here, we show a comprehensive profile of antibody, B cell and T cell dynamics over time in a cohort of patients who have recovered from mild-moderate COVID-19. Binding and neutralising antibody responses, together with individual serum clonotypes, decay over the first 4 months post-infection. A similar decline in Spike-specific CD4 + and circulating T follicular helper frequencies occurs. By contrast, S-specific IgG + memory B cells consistently accumulate over time, eventually comprising a substantial fraction of circulating the memory B cell pool. Modelling of the concomitant immune kinetics predicts maintenance of serological neutralising activity above a titre of 1:40 in 50% of convalescent participants to 74 days, although there is probably additive protection from B cell and T cell immunity. This study indicates that SARS-CoV-2 immunity after infection might be transiently protective at a population level. Therefore, SARS-CoV-2 vaccines might require greater immunogenicity and durability than natural infection to drive long-term protection.


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