ArticleProceedings of the National Academy of Sciences of the United States of America2023
Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Secreted ORF8 reprograms macrophages to enhance SARS-CoV-2 infection of lung epithelial cells.Science advances · 2026Article
- Implications of RNA virus persistence for post-acute sequelae and chronic inflammatory syndromes.Nature immunology · 2026Review
- COVID-19 Is Airborne AIDS: Provocative Oversimplification, Emerging Science, or Something in Between?AJPM focus · 2026Review
- Secreted ORF8 reprograms macrophages to enhance SARS-CoV-2 infection of lung epithelial cells.bioRxiv : the preprint server for biology · 2026Article
- Targeting SARS-CoV-2 Structural and Accessory Proteins: Emerging Opportunities for Small-Molecule Coronavirus Antivirals.Pharmaceutics · 2026Review
- Review
- HLA-C-derived peptide MH-1 as an early-stage intervention against SARS-CoV-2 infection.Molecular medicine (Cambridge, Mass.) · 2026Article
- The race between viral immune evasion and the MHC class I antigen processing pathway.FEMS microbiology reviews · 2026Review
- SARS-CoV-2 variants: biology, pathogenicity, immunity and control.Nature reviews. Microbiology · 2026Review
- SARS-CoV-2 ORF8: an accessory protein at the interface of immune evasion and inflammation.Frontiers in immunology · 2026Review
- LMP7 as a Target for Coronavirus Therapy: Inhibition by Ixazomib and Interaction with SARS-CoV-2 Proteins Nsp13 and Nsp16.Pathogens (Basel, Switzerland) · 2025Article
- Epithelial Memory After Respiratory Viral Infection in Mice Results in Prolonged Enhancement of Antigen Presentation.Allergy · 2025Article
- Article
- The Recurring Loss of ORF8 Secretion in Dominant SARS-CoV-2 Variants.International journal of molecular sciences · 2025Article
- Programmed cell death markers in COVID-19 survivors with and without sepsis.Frontiers in immunology · 2025Article
- Predicting pathogen evolution and immune evasion in the age of artificial intelligence.Computational and structural biotechnology journal · 2025Review
- Intranasal Multiepitope PD-L1-siRNA-Based Nanovaccine: The Next-Gen COVID-19 Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cholesterol and Cholesterol-Lowering Medications in COVID-19-An Unresolved Matter.International journal of molecular sciences · 2024Review
- Review
- SARS-CoV-2-related bat viruses evade human intrinsic immunity but lack efficient transmission capacity.Nature microbiology · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.