Abstract
So far, it is impossible to explain the diverse individual and population responses to SARS-CoV-2 infection. Many factors may be involved, including genetics, diet, vaccinations, the innate immune response, viral load, and other phenomena. Further, immune responses raised against pathogens other than SARS-CoV-2 (cross-reactivity) may also be involved. In this work, we analyzed the potential for T-cell cross-reactivity between less contagious coronaviruses (HCoV-OC43, HCoV-HKU1, HCoV-229E, and HCoV-NL63) and SARS-CoV-2. In silico research suggests that SARS-CoV-2 and less dangerous coronaviruses share identical peptides, which can be presented on MHC class I molecules. Those T-cells epitopes belong to several coronavirus proteins localized inside the viral envelope, including helicase, RNA polymerase, proofreading exoribonuclease, and 2'-O-methyltransferase. Our data suggest that a milder course of COVID-19, in some populations, may be related to the cross-reactivity of T cells.