ArticlePLoS pathogens2019
Varicella zoster virus productively infects human peripheral blood mononuclear cells to modulate expression of immunoinhibitory proteins and blocking PD-L1 enhances virus-specific CD8+ T cell effector function.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Efficacy of Immune Checkpoint Inhibitors and Oncoviruses in Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Prevalence of VZV Reactivation and Effectiveness of Vaccination with Recombinant Adjuvanted Zoster Vaccine in Allogeneic Hematopoietic Stem Cell Recipients-A Single-Center Analysis.Infectious disease reports · 2025Article
- Article
- Analysis of single-cell and spatial transcriptomics in TNBC cell-cell interactions.Frontiers in immunology · 2025Review
- Transplant international : official journal of the European Society for Organ Transplantation · 2025Article
- CD4/CD8 Ratio: An Independent Predictor of Herpes Zoster in Patients With Autoimmune Inflammatory Rheumatic Diseases.Annals of dermatology · 2024Article
- PD-L1/PD-1 pathway: a potential neuroimmune target for pain relief.Cell & bioscience · 2024Review
- Article
- Inhibition of SFTSV replication in humanized mice by a subcutaneously administered anti-PD1 nanobody.EMBO molecular medicine · 2024Article
- Impaired STING Activation Due to a Variant in the E3 Ubiquitin Ligase AMFR in a Patient with Severe VZV Infection and Hemophagocytic Lymphohistiocytosis.Journal of clinical immunology · 2024Article
- The immunogenicity and the safety of the adjuvanted glycoprotein E (gE)-based recombinant vaccine against herpes zoster (RZV) in cancer patients during immunotherapy.Human vaccines & immunotherapeutics · 2023Article
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Varicella Zoster Virus infects mucosal associated Invariant T cells.Frontiers in immunology · 2023Article
- Review
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Article
- Development of a skin- and neuro-attenuated live vaccine for varicella.Nature communications · 2022Article
- Molecular mechanisms governing circulating immune cell heterogeneity across different species revealed by single-cell sequencing.Clinical and translational medicine · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Varicella zoster virus (VZV) is a lymphotropic alpha-herpesvirinae subfamily member that produces varicella on primary infection and causes zoster, vascular disease and vision loss upon reactivation from latency. VZV-infected peripheral blood mononuclear cells (PBMCs) disseminate virus to distal organs to produce clinical disease. To assess immune evasion strategies elicited by VZV that may contribute to dissemination of infection, human PBMCs and VZV-specific CD8+ T cells (V-CD8+) were mock- or VZV-infected and analyzed for immunoinhibitory protein PD-1, PD-L1, PD-L2, CTLA-4, LAG-3 and TIM-3 expression using flow cytometry. All VZV-infected PBMCs (monocytes, NK, NKT, B cells, CD4+ and CD8+ T cells) and V-CD8+ showed significant elevations in PD-L1 expression compared to uninfected cells. VZV induced PD-L2 expression in B cells and V-CD8+. Only VZV-infected CD8+ T cells, NKT cells and V-CD8+ upregulated PD-1 expression, the immunoinhibitory receptor for PD-L1/PD-L2. VZV induced CTLA-4 expression only in V-CD8+ and no significant changes in LAG-3 or TIM-3 expression were observed in V-CD8+ or PBMC T cells. To test whether PD-L1, PD-L2 or CTLA-4 regulates V-CD8+ effector function, autologous PBMCs were VZV-infected and co-cultured with V-CD8+ cells in the presence of blocking antibodies against PD-L1, PD-L2 or CTLA-4; ELISAs revealed significant elevations in IFNγ only upon blocking of PD-L1. Together, these results identified additional immune cells that are permissive to VZV infection (monocytes, B cells and NKT cells); along with a novel mechanism for inhibiting CD8+ T cell effector function through induction of PD-L1 expression.
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