| Description: |
Since the first news about the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) appeared, a large amount of data on the variability of the virus genome have accumulated. Most of the mutations entrenched in the viral genome are aimed at improving the mechanisms of host cell penetration, altering the degree of binding to protein receptors, evading the immune system, and suppressing the antiviral immune response. Knowledge of the functional role of mutations will allow improving diagnostic methods, treatment, and vaccine prophylaxis regimens, as well as predicting the further spread and evolution of the virus. In this study, we analyzed a number of SARS-CoV-2 virus mutations in the context of viral epitope affinity for most common in Russia HLA class I and class II alleles (according to Allele Frequency Net Database). This study examined clade-forming mutations of viral clades that are classified as variants of concern according to the WHO classification. We found that some mutations reduce the number of predicted epitopes, the number of HLA alleles that bind them, or the number of both epitopes and HLA alleles simultaneously. Mutations of the viral clade B.1.1.7 (S:Y144del, S:H69-V70del, and S:A570D), mutations of the viral clade B.1.617.2 (S:T19R, S:G12D, S:F157del, and S:R158del), and mutation N:R203K related to all clades except B.1.617.2 have pronounced effects on reducing epitope affinity for HLA alleles, with some of them affecting on epitopes of all the studied strong and weak binders lengths in both HLA class I and class II. |