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First Author:  Guthmiller et al. 

Journal/preprint name: BioRxiv 

Paper DOIhttps://doi.org/10.1101/2020.09.12.294066.  

Tags:  Bioinformatics, Clinical, Immunology/Immunity 

Summary  

Guthmiller et al. evaluate plasma from hospitalised acutely SARS-CoV-2 infected and convalescent subjects. The antibody response against SARS-CoV-2 was present in the majority of patients and largely driven against the nucleocapsid (Nfirst) and spike (Slater) proteins, with response to other antigens mainly found during acute infection. Disease severity was correlated with increased antibody titers in both acute and convalescent subjects. In acute infection, those hospitalised longer mounted a larger antibody response against N and were more likely to mount a response against other SARS-CoV-2 antigens, like ORF8 and NSP. Among convalescent subjects, high responders had high titers against N but also ORF8. Memory B cells from convalescent subjects largely targeted S and correlated with antibody titers against S but not against N. The antibodies against S appeared to target conserved epitopes, and reacted with S with the D614G mutation and cross-reacted with SARS-CoV-1 receptor binding domainOverall, this preprint shows that disease severity directly correlates with the breadth and magnitude of the humoral immune response. 

Research Highlights 

  1. Subjects with a more severe SARS-CoV-2 infection exhibit a larger antibody response mainly directed against and N, but also ORF8 and NSP.  

  1. Greater antibody response correlated with a larger memory B cell response against S, but not N 

  1. Antibodies against S can bind the D614G mutant and cross-react with the SARS-CoV-1 receptor binding domain 

Impact for COVID-19 research:  

  • Helps understand the humoral immune response 

Methodologies: 

  • Study Typeclinical samples, ex vivo 

  • Important cell lines/viral models used: Clinical samples 

  • Key Techniques: Bioinformatics, ELISpot, Neutralisation assays, ELISA 

Limitations: 

  • Neither the neutralizing capacity nor the role of the antibodies in pathogenesis is addressed, but the authors comment on that.  

  • A link on the viral titers and the magnitude of the antibody response would have been a complementary and less biased measure than length of hospitalisation. But the authors mention in the discussion that length on hopitalisation may link to viral titers. 

  • There is no information on whether of those hospitalised, all resolved the infection or some died, and in which case if the response was found to be different.  

  • It would have been informative to evaluate acute asymptomatic SARS-CoV-2 infected subjects. 

  • The conclusions are similar to a number of previous studies