ArticleJournal of virology2008
Vesicular stomatitis virus oncolysis of T lymphocytes requires cell cycle entry and translation initiation.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Multiple RNA virus matrix proteins interact with SLD5 to manipulate host cell cycle.The Journal of general virology · 2021Article
- Enhanced Safety and Efficacy of Oncolytic VSV Therapy by Combination with T Cell Receptor Transgenic T Cells as Carriers.Molecular therapy oncolytics · 2019Article
- Cell Cycle Arrest in GJournal of virology · 2019Article
- The Oncolytic Virus MG1 Targets and Eliminates Cells Latently Infected With HIV-1: Implications for an HIV Cure.The Journal of infectious diseases · 2018Article
- Quantitative profiling of innate immune activation by viral infection in single cells.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- VSV based virotherapy in ovarian cancer: the past, the present and …future?Journal of Cancer · 2017Review
- Retargeting Oncolytic Vesicular Stomatitis Virus to Human T-Cell Lymphotropic Virus Type 1-Associated Adult T-Cell Leukemia.Journal of virology · 2015Article
- Oncolytic viruses: From bench to bedside with a focus on safety.Human vaccines & immunotherapeutics · 2015Review
- From scourge to cure: tumour-selective viral pathogenesis as a new strategy against cancer.PLoS pathogens · 2014Review
- Antiglioma oncolytic virotherapy: unattainable goal or a success story in the making?Future virology · 2013Article
- Targeting and killing of metastatic cells in the transgenic adenocarcinoma of mouse prostate model with vesicular stomatitis virus.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Tinkering with translation: protein synthesis in virus-infected cells.Cold Spring Harbor perspectives in biology · 2013Review
- Vesicular stomatitis virus as a flexible platform for oncolytic virotherapy against cancer.The Journal of general virology · 2012Review
- Reduced Newcastle disease virus-induced oncolysis in a subpopulation of cisplatin-resistant MCF7 cells is associated with survivin stabilization.Cancer cell international · 2012Article
- Oncolytic virotherapy.Nature biotechnology · 2012Review
- Posttranslational modification of vesicular stomatitis virus glycoprotein, but not JNK inhibition, is the antiviral mechanism of SP600125.Journal of virology · 2012Article
- TLR2 activation enhances HIV nuclear import and infection through T cell activation-independent and -dependent pathways.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Enhancing VSV oncolytic activity with an improved cytosine deaminase suicide gene strategy.Cancer gene therapy · 2011Article
- Cell cycle progression or translation control is not essential for vesicular stomatitis virus oncolysis of hepatocellular carcinoma.PloS one · 2010Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Vesicular stomatitis virus (VSV) is a candidate oncolytic virus that replicates and induces cell death in cancer cells while sparing normal cells. Although defects in the interferon antiviral response facilitate VSV oncolysis, other host factors, including translational and growth regulatory mechanisms, also appear to influence oncolytic virus activity. We previously demonstrated that VSV infection induces apoptosis in proliferating CD4(+) T lymphocytes from adult T-cell leukemia samples but not in resting T lymphocytes or primary chronic lymphocytic leukemia cells that remain arrested in G(0). Activation of primary CD4(+) T lymphocytes with anti-CD3/CD28 is sufficient to induce VSV replication and cell death in a manner dependent on activation of the MEK1/2, c-Jun NH(2)-terminal kinase, or phosphatidylinositol 3-kinase pathway but not p38. VSV replication is specifically impaired by the cell cycle inhibitor olomoucine or rapamycin, which induces early G(1) arrest, but not by aphidicolin or Taxol, which blocks at the G(1)1S or G(2)1M phase, respectively; this result suggests a requirement for cell cycle entry for efficient VSV replication. The relationship between increased protein translation following G(0)/G(1) transition and VSV permissiveness is highlighted by the absence of mTOR and/or eIF4E phosphorylation whenever VSV replication is impaired. Furthermore, VSV protein production in activated T cells is diminished by small interfering RNA-mediated eIF4E knockdown. These results demonstrate that VSV replication in primary T lymphocytes relies on cell cycle transition from the G(0) phase to the G(1) phase, which is characterized by a sharp increase in ribogenesis and protein synthesis.
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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.