iScience · 2025
Mutational pressure promotes release of public CD8+ T cell epitopes by proteasome from SARS-CoV-2 RBD of Omicron and its current lineages.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kudriaeva Anna A, Butenko Ivan O, Saratov George A, Ri Maxim Т, Mokrushina Yuliana A, Bondarev Alexey A, Evpak Alena S, Smirnov Ivan V, Matyushkina Daria S, Gabibov Alexander G, Govorun Vadim M, Belogurov Alexey A
Аннотация
The COVID-19 pandemic was the most dramatic in the newest history with nearly 7 million deaths and global impact on mankind. Here, we report binding index of 305 human leukocyte antigen (HLA) class I molecules from 18,771 unique haplotypes of 28,104 individuals to 821 peptides experimentally observed from spike protein receptor binding domain (RBD) of five main SARS-CoV-2 strains hydrolyzed by human proteasomes with constitutive and immune catalytic phenotypes. Our data read that mutations in the human angiotensin-converting enzyme 2 (hACE2)-binding region RBD496-513 of Omicron B.1.1.529 strain results in a dramatic increase of proteasome-mediated release of two public HLA class I epitopes. Global population analysis of HLA class I haplotypes, specific to these peptides, demonstrated decreased mortality of human populations enriched in these haplotypes from COVID-19 after but not before December, 2021, when Omicron became dominant SARS-CoV-2 strain. Noteworthy, currently circulating BA.2.86 and JN.1 strains contain same amino acid substitutions at key proteasomal cleavage sites, thus preserving identified core epitopes.