ArticleJournal of virology2011
Mutations in the glycoprotein of vesicular stomatitis virus affect cytopathogenicity: potential for oncolytic virotherapy.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Resistance signatures to oncolytic vesiculoviruses in pancreatic ductal adenocarcinoma.Molecular therapy. Oncology · 2025Article
- Oncolytic viruses: A novel treatment strategy for breast cancer.Genes & diseases · 2023Review
- Article
- Creation of a synthesis-friendly inflammation-inducible promoter suitable for cell therapy.Integrative biology : quantitative biosciences from nano to macro · 2021Article
- Review
- Altered expression of fractalkine in HIV-1-infected astrocytes and consequences for the virus-related neurotoxicity.Journal of neurovirology · 2021Article
- Experimental virus evolution in cancer cell monolayers, spheroids, and tissue explants.Virus evolution · 2021Article
- Experimental Evolution Generates Novel Oncolytic Vesicular Stomatitis Viruses with Improved Replication in Virus-Resistant Pancreatic Cancer Cells.Journal of virology · 2020Article
- M51R and Delta-M51 matrix protein of the vesicular stomatitis virus induce apoptosis in colorectal cancer cells.Molecular biology reports · 2019Article
- Review
- Increased Virulence of an Epidemic Strain of Vesicular Stomatitis Virus Is Associated With Interference of the Innate Response in Pigs.Frontiers in microbiology · 2018Article
- Oncolytic Vesicular Stomatitis Virus as a Viro-Immunotherapy: Defeating Cancer with a "Hammer" and "Anvil".Biomedicines · 2017Review
- Changes in Susceptibility to Oncolytic Vesicular Stomatitis Virus during Progression of Prostate Cancer.Journal of virology · 2015Article
- The strength of the T cell response against a surrogate tumor antigen induced by oncolytic VSV therapy does not correlate with tumor control.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Experimental evolution of an oncolytic vesicular stomatitis virus with increased selectivity for p53-deficient cells.PloS one · 2014Article
- How Informative is the Immune Response Against Surrogate Tumor Antigens to Assess Antitumor Immunity?Frontiers in oncology · 2014Article
- Cancer upregulated gene 2, a novel oncogene, confers resistance to oncolytic vesicular stomatitis virus through STAT1-OASL2 signaling.Cancer gene therapy · 2013Article
- Vesicular stomatitis virus as a flexible platform for oncolytic virotherapy against cancer.The Journal of general virology · 2012Review
- Relationship between within-host fitness and virulence in the vesicular stomatitis virus: correlation with partial decoupling.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Vesicular stomatitis virus (VSV) has been widely used to characterize cellular processes, viral resistance, and cytopathogenicity. Recently, VSV has also been used for oncolytic virotherapy due to its capacity to selectively lyse tumor cells. Mutants of the matrix (M) protein of VSV have generally been preferred to the wild-type virus for oncolysis because of their ability to induce type I interferon (IFN) despite causing weaker cytopathic effects. However, due to the large variability of tumor types, it is quite clear that various approaches and combinations of multiple oncolytic viruses will be needed to effectively treat most cancers. With this in mind, our work focused on characterizing the cytopathogenic profiles of four replicative envelope glycoprotein (G) VSV mutants. In contrast to the prototypic M mutant, VSV G mutants are as efficient as wild-type virus at inhibiting cellular transcription and host protein translation. Despite being highly cytopathic, the mutant G(6R) triggers type I interferon secretion as efficiently as the M mutant. Importantly, most VSV G mutants are more effective at killing B16 and MC57 tumor cells in vitro than the M mutant or wild-type virus through apoptosis induction. Taken together, our results demonstrate that VSV G mutants retain the high cytopathogenicity of wild-type VSV, with G(6R) inducing type I IFN secretion at levels similar to that of the M mutant. VSV G protein mutants could therefore prove to be highly valuable for the development of novel oncolytic virotherapy strategies that are both safe and efficient for the treatment of various types of cancer.
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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.