• Media type: E-Article
  • Title: Older adults lack SARS CoV-2 cross-reactive T lymphocytes directed to human coronaviruses OC43 and NL63
  • Contributor: Saletti, Giulietta; Gerlach, Thomas; Jansen, Janina M.; Molle, Antonia; Elbahesh, Husni; Ludlow, Martin; Li, Wentao; Bosch, Berend-Jan; Osterhaus, Albert D. M. E.; Rimmelzwaan, Guus F.
  • imprint: Springer Science and Business Media LLC, 2020
  • Published in: Scientific Reports
  • Language: English
  • DOI: 10.1038/s41598-020-78506-9
  • ISSN: 2045-2322
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>Currently, 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 &gt; 60 years of age account for &gt; 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.</jats:p>
  • Access State: Open Access