ArticleThe Journal of infectious diseases2023
Varicella Zoster Virus Impairs Expression of the Nonclassical Major Histocompatibility Complex Class I-Related Gene Protein (MR1).
Article in The Journal of infectious diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Allelic variation alters expression and antigen presentation of MR1 allomorphs.The Journal of biological chemistry · 2026Article
- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- Varicella Zoster Virus Downregulates Expression of the Nonclassical Antigen Presentation Molecule CD1d.The Journal of infectious diseases · 2024Article
- Varicella Zoster Virus disrupts MAIT cell polyfunctional effector responses.PLoS pathogens · 2024Article
- MR1 antigen presentation to MAIT cells and other MR1-restricted T cells.Nature reviews. Immunology · 2024Review
- Multi-targeted loss of the antigen presentation molecule MR1 during HSV-1 and HSV-2 infection.iScience · 2024Article
- The Emerging Role of MAIT Cell Responses in Viral Infections.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Targeting the MR1-MAIT cell axis improves vaccine efficacy and affords protection against viral pathogens.PLoS pathogens · 2023Article
- Suppression of MR1 by human cytomegalovirus inhibits MAIT cell activation.Frontiers in immunology · 2023Article
- Editorial: MAIT cells come of age.Frontiers in immunology · 2023Article
- Varicella Zoster Virus infects mucosal associated Invariant T cells.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
The antigen presentation molecule MR1 (major histocompatibility complex, class I-related) presents ligands derived from the riboflavin (vitamin B) synthesis pathway, which is not present in mammalian species or viruses, to mucosal-associated invariant T (MAIT) cells. In this study, we demonstrate that varicella zoster virus (VZV) profoundly suppresses MR1 expression. We show that VZV targets the intracellular reservoir of immature MR1 for degradation, while preexisting, ligand-bound cell surface MR1 is protected from such targeting, thereby highlighting an intricate temporal relationship between infection and ligand availability. We also identify VZV open reading frame (ORF) 66 as functioning to suppress MR1 expression when this viral protein is expressed during transient transfection, but this is not apparent during infection with a VZV mutant virus lacking ORF66 expression. This indicates that VZV is likely to encode multiple viral genes that target MR1. Overall, we identify an immunomodulatory function of VZV whereby infection suppresses the MR1 biosynthesis pathway.
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Registered trials
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.