The recent COVID-19 pandemic left behind the lingering question of whether new variants of concern might cause further waves of infection. So, it is important to investigate the long-term protection provided by vaccination or exposure to the SARS-CoV-2 virus.
T cells are key players in the immune response to viral infection, forming a memory to the virus so that recurrent infections can be more rapidly cleared. In this study, the research team compared the long-term memory T-cell responses following infection with the virus itself, followed by subsequent infections and vaccinations.
They identified common public T cell receptors that are used by dominant SARS-CoV-2 T cells, associated with mild disease outcome, and likely play important protective roles in subsequent viral infection events.
Their analysis focused on the specific responses against three SARS-CoV-2 protein targets - responses that have previously been shown to be found in a large proportion of the population. Analysis of the receptors on the surface of the T cells identified specific receptors shared amongst many different individuals, which the researchers found to be associated with mild COVID-19, compared to those without this receptor who had more severe disease. Furthermore, these specific receptors were found in individuals analysed before the COVID-19 pandemic, suggesting their existence before the pandemic may have allowed these cells to respond quicker to the virus once encountered.
Further investigation of the function of these cells revealed that 3-4 years after infection, the cells exhibited greater cytotoxic potential compared to cells 1-3 months after infection, which was associated with the ability of these cells to suppress the replication of the virus.
Professor Tao Dong, Co-Director of the CAMS Oxford Institute and corresponding author on the study, said:
In this study, we have demonstrated that SARS-CoV-2 spike-specific CD4+ T-cells with public TCR usage, reflecting high precursor frequencies, were associated with milder COVID-19 disease and with increased cytotoxicity four years post COVID-19, suggesting their important protective roles in subsequent viral infection events.
Read the full paper on the Nature Communications website: