Article ; Online: Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants.
Proceedings of the National Academy of Sciences of the United States of America
2023 Volume 120, Issue 16, Page(s) e2221652120
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern (VOCs) possess mutations that confer resistance to neutralizing antibodies within the Spike protein and are associated with breakthrough infection and reinfection. By ... ...
Abstract | Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern (VOCs) possess mutations that confer resistance to neutralizing antibodies within the Spike protein and are associated with breakthrough infection and reinfection. By contrast, less is known about the escape from CD8+ T cell-mediated immunity by VOC. Here, we demonstrated that all SARS-CoV-2 VOCs possess the ability to suppress major histocompatibility complex class I (MHC-I) expression. We identified several viral genes that contribute to the suppression of MHC I expression. Notably, MHC-I upregulation was strongly inhibited after SARS-CoV-2 but not influenza virus infection in vivo. While earlier VOCs possess similar capacity as the ancestral strain to suppress MHC-I, the Omicron subvariants exhibited a greater ability to suppress surface MHC-I expression. We identified a common mutation in the E protein of Omicron that further suppressed MHC-I expression. Collectively, our data suggest that in addition to escaping from neutralizing antibodies, the success of Omicron subvariants to cause breakthrough infection and reinfection may in part be due to its optimized evasion from T cell recognition. |
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MeSH term(s) | Humans ; Antibodies, Neutralizing ; Antibodies, Viral ; Breakthrough Infections ; COVID-19/genetics ; Reinfection ; SARS-CoV-2/genetics ; Spike Glycoprotein, Coronavirus/genetics |
Chemical Substances | Antibodies, Neutralizing ; Antibodies, Viral ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 |
Language | English |
Publishing date | 2023-04-10 |
Publishing country | United States |
Document type | Journal Article ; Research Support, N.I.H., Extramural |
ZDB-ID | 209104-5 |
ISSN | 1091-6490 ; 0027-8424 |
ISSN (online) | 1091-6490 |
ISSN | 0027-8424 |
DOI | 10.1073/pnas.2221652120 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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