ArticlePLoS pathogens2024
Varicella Zoster Virus disrupts MAIT cell polyfunctional effector responses.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Gastrointestinal MAIT cells in chronic HIV-1 infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- The immune response to human cytomegalovirus: impact of age, co-morbidities and the significance of anti-viral activity assessment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- The global burden of varicella and herpes zoster in adults aged 65 years and older: a comprehensive analysis based on the global burden of disease 2021.Aging clinical and experimental research · 2025Article
- Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Mucosal-associated invariant T (MAIT) cells are unconventional T cells that respond to riboflavin biosynthesis and cytokines through TCR-dependent and -independent pathways, respectively. MAIT cell activation plays an immunoprotective role against several pathogens, however the functional capacity of MAIT cells following direct infection or exposure to infectious agents remains poorly defined. We investigated the impact of Varicella Zoster Virus (VZV) on blood-derived MAIT cells and report virus-mediated impairment of activation, cytokine production, and altered transcription factor expression by VZV infected (antigen+) and VZV exposed (antigen-) MAIT cells in response to TCR-dependent and -independent stimulation. Furthermore, we reveal that suppression of VZV exposed (antigen-) MAIT cells is not mediated by a soluble factor from neighbouring VZV infected (antigen+) MAIT cells. Finally, we demonstrate that VZV impairs the cytolytic potential of MAIT cells in response to riboflavin synthesising bacteria. In summary, we report a virus-mediated immune-evasion strategy that disarms MAIT cell responses.
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Registered trials
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