ArticlePloS one2011
Vesicular stomatitis virus infection promotes immune evasion by preventing NKG2D-ligand surface expression.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Characterisation and Sensitivity of a Canine Mast Cell Tumour Line to Oncolytic Viruses.Veterinary and comparative oncology · 2025Article
- Whole-transcriptome analysis of BLV-infected cows reveals downregulation of immune response genes in high proviral loads cows.Frontiers in veterinary science · 2025Article
- Computational prediction of intracellular targets of wild-type or mutant vesicular stomatitis matrix protein.PloS one · 2022Article
- Review
- Oncolytic Viro-Immunotherapy: An Emerging Option in the Treatment of Gliomas.Frontiers in immunology · 2021Review
- Review
- Rapid dose-dependent Natural Killer (NK) cell modulation and cytokine responses following human rVSV-ZEBOV Ebolavirus vaccination.NPJ vaccines · 2020Article
- Natural killer group 2D receptor and its ligands in cancer immune escape.Molecular cancer · 2019Review
- NKG2D and Its Ligands: "One for All, All for One".Frontiers in immunology · 2018Review
- Oncolytic measles virus enhances antitumour responses of adoptive CD8Scientific reports · 2017Article
- Viral Evasion of Natural Killer Cell Activation.Viruses · 2016Review
- Concise review: immunologic lessons from solid organ transplantation for stem cell-based therapies.Stem cells translational medicine · 2013Review
- NKG2D ligands as therapeutic targets.Cancer immunity · 2013Review
- Vesicular stomatitis virus as a flexible platform for oncolytic virotherapy against cancer.The Journal of general virology · 2012Review
- Elevation of soluble major histocompatibility complex class I related chain A protein in malignant and infectious diseases in Chinese patients.BMC immunology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection leads to a robust induction of MICA mRNA expression, however the subsequent surface expression is potently hindered. Thus, VSV lines up with human cytomegalovirus (HCMV) and adenovirus, which actively subvert the immune system by negatively affecting NKG2D-ligand surface expression. VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression. The classical immune escape mechanism of VSV (i.e., the M protein blockade of nucleocytoplasmic mRNA transport) was not involved, as the VSV mutant strain, VSV(ΔM51), which possess a defective M protein, prevented MICA surface expression similarly to wild-type VSV. The VSV mediated down modulation of NKG2D-ligand expression did not involve apoptosis. Constitutive expression of MICA bypassed the escape mechanism, suggesting that VSV affect NKG2D-ligand expression at an early post-transcriptional level. Our results show that VSV possess an escape mechanism, which could affect the immune recognition of VSV infected cancer cells. This may also have implications for immune recognition of cancer cells after combined treatment with VSV and chemotherapeutic drugs.
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