The rapid emergence of SARS-CoV-2 and the ensuing pandemic shifted research focus towards severe COVID-19 cases, with relatively little attention given to understanding why about 20% of infected individuals remain asymptomatic. Our study unravelled the natural immunity that shields asymptomatic individuals from COVID symptoms.
T lymphocyte activation is driven by the recognition of Human Leukocyte Antigens (HLA) on the surface infected cells. HLAs present viral peptides to T cells, which then recognize them as antigens via their T cell receptor (TCR). However, the polymorphic nature of HLA molecules leads to variations in the adaptive immune response. We discovered a link between asymptomatic COVID infection and a specific HLA, HLA-B*15:01, which is present in approximately 3% of the global population. We sought to understand how HLA-B*15:01 provided protection against SARS-CoV-2.
We examined four SARS-CoV-2-derived epitopes that could be presented by HLA-B*15:01 using samples collected in the 90’s before the COVID-19 pandemic. These individuals were unexposed to the virus, not vaccinated, and not even exposed to SARS-CoV-1. One epitope, NQK-Q8, from the spike protein, triggered a robust memory T cell response in unexposed individuals. Interestingly a homologous peptide, NQK-A8, from human seasonal coronaviruses, was recognized by the same T cells. I showed that HLA-B*15:01 was able to present the two peptides with similar stability and using X-ray crystallography, we found that the residue difference at position 8 of the peptides were solvent-exposed and could be a contact point for T cells.
We show that both epitopes efficiently activate T cells and assessed the affinity of T cell receptors (TCRs) isolated from COVID-recovered, vaccinated, and unexposed HLA-B*15:01+ individuals exhibited. The TCRs had a high and similar affinity for both peptides. and facilitate viral recognition and protection in HLA-B*15:01+ individuals.
This discovery not only enhances our understanding of the immunological factors behind the potential rapid viral clearance but also provides a foundation for developing therapeutics that would mimic such a protective immune response as observed in HLA-B*15:01+ individuals.
This work has been published in Nature (Augusto et al. 2023)