• Giulietta Saletti, Thomas Gerlach, Janina M Jansen, Antonia Molle, Husni Elbahesh, Martin Ludlow, Wentao Li, Berend-Jan Bosch, OsterhausAlbert D M EADMEResearch Center for Emerging Infections and Zoonoses, University of Veterinary Medicine, Bünteweg 17, 30559, Hannover, Germany., and Guus F Rimmelzwaan.
• Research Center for Emerging Infections and Zoonoses, University of Veterinary Medicine, Bünteweg 17, 30559, Hannover, Germany.
• Sci Rep. 2020 Dec 8; 10 (1): 21447.

AbstractCurrently, infections with SARS-Coronavirus-2 (SARS-CoV-2), the causative agent of the COVID-19 pandemic, are responsible for substantial morbidity and mortality worldwide. Older adults subjects > 60 years of age account for > 95% of the over one million fatal cases reported to date. It is unclear why in this age group SARS-CoV-2 infection causes more severe disease than in young adults. We hypothesized that differences in SARS-CoV-2 cross-reactive cellular immunity induced after infection with human coronaviruses (HCoVs), like OC43 and NL63, were at the basis of the differential mortality (and morbidity) observed after SARS-CoV-2 infection, because a small proportion of HCoV-specific T cells cross-react with SARS-CoV-2. Our data demonstrate that pre-existing T cell immunity induced by circulating human alpha- and beta-HCoVs is present in young adult individuals, but virtually absent in older adult subjects. Consequently, the frequency of cross-reactive T cells directed to the novel pandemic SARS-CoV-2 was minimal in most older adults. To the best of our knowledge, this is the first time that the presence of cross-reactive T cells to SARS-CoV-2 is compared in young and older adults. Our findings provide at least a partial explanation for the more severe clinical outcome of SARS-CoV-2 infection observed in the elderly. Moreover, this information could help to design efficacious vaccines for this age group, aiming at the induction of cell-mediated immunity.

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