ArticleGene therapy2013
Expression of HSV-1 receptors in EBV-associated lymphoproliferative disease determines susceptibility to oncolytic HSV.
Article in Gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Efficacy of a third-generation oncolytic herpes simplex virus in refractory soft tissue sarcoma xenograft models.Molecular therapy oncolytics · 2022Article
- Oncolytic herpes simplex virus infects myeloma cellsMolecular therapy oncolytics · 2021Article
- Oncolytic Virus Therapy with HSV-1 for Hematological Malignancies.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Enhanced Sensitivity of Patient-Derived Pediatric High-Grade Brain Tumor Xenografts to Oncolytic HSV-1 Virotherapy Correlates with Nectin-1 Expression.Scientific reports · 2018Article
- Third-generation oncolytic herpes simplex virus inhibits the growth of liver tumors in mice.Cancer science · 2018Article
- Neuroblastomas vary widely in their sensitivities to herpes simplex virotherapy unrelated to virus receptors and susceptibility.Gene therapy · 2016Article
- Histone deacetylase 6 inhibition enhances oncolytic viral replication in glioma.The Journal of clinical investigation · 2015Article
- Oncolytic HSV virotherapy in murine sarcomas differentially triggers an antitumor T-cell response in the absence of virus permissivity.Molecular therapy oncolytics · 2015Article
- Assessment of oncolytic HSV efficacy following increased entry-receptor expression in malignant peripheral nerve sheath tumor cell lines.Gene therapy · 2014Article
- Epithelial-mesenchymal transition enhances response to oncolytic herpesviral therapy through nectin-1.Human gene therapy · 2014Article
- Pediatric cancer gone viral. Part I: strategies for utilizing oncolytic herpes simplex virus-1 in children.Molecular therapy oncolyticsArticle
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Epstein-Barr virus (EBV)-associated B-cell lymphoproliferative disease (LPD) after hematopoietic stem cell or solid organ transplantation remains a life-threatening complication. Expression of the virus-encoded gene product, EBER, has been shown to prevent apoptosis via blockade of PKR activation. As PKR is a major cellular defense against Herpes simplex virus (HSV), and oncolytic HSV-1 (oHSV) mutants have shown promising antitumor efficacy in preclinical models, we sought to determine whether EBV-LPD cells are susceptible to infection by oHSVs. We tested three primary EBV-infected lymphocyte cell cultures from neuroblastoma (NB) patients as models of naturally acquired EBV-LPD. NB12 was the most susceptible, NB122R was intermediate and NB88R2 was essentially resistant. Despite EBER expression, PKR was activated by oHSV infection. Susceptibility to oHSV correlated with the expression of the HSV receptor, nectin-1. The resistance of NB88R2 was reversed by exogenous nectin-1 expression, whereas downregulation of nectin-1 on NB12 decreased viral entry. Xenografts derived from the EBV-LPDs exhibited only mild (NB12) or no (NB88R2) response to oHSV injection, compared with a NB cell line that showed a significant response. We conclude that EBV-LPDs are relatively resistant to oHSV virotherapy, in some cases, due to low virus receptor expression but also due to intact antiviral PKR signaling.
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