In silico studies suggest T-cell cross-reactivity between SARS-CoV-2 and less dangerous coronaviruses
Marcin Pacholczyk, Piotr Rieske
Received date: 7th September 2020
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.
This is an abstract of a preprint hosted on a preprint server, which is currently undergoing peer review at Scientific Reports. The findings have yet to be thoroughly evaluated, nor has a decision on ultimate publication been made. Therefore, the results reported should not be considered conclusive, and these findings should not be used to inform clinical practice, or public health policy, or be promoted as verified information.