ArticleProceedings of the National Academy of Sciences of the United States of America2006
Construction and properties of a herpes simplex virus 1 designed to enter cells solely via the IL-13alpha2 receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
56 citing papers in PubMed, 72 citations in OpenAlex.
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Novel mutations in UMolecular therapy. Methods & clinical development · 2023Article
- The IL13α 2R paves the way for anti-glioma nanotherapy.Genes & diseases · 2023Review
- Nanobody-based retargeting of an oncolytic herpesvirus for eliminating CXCR4Molecular therapy oncolytics · 2022Article
- Implications of immune cells in oncolytic herpes simplex virotherapy for glioma.Brain tumor pathology · 2022Review
- Herpes simplex virus 1 as an oncolytic viral therapy for refractory cancers.Frontiers in oncology · 2022Review
- Potent anti-tumor effects of receptor-retargeted syncytial oncolytic herpes simplex virus.Molecular therapy oncolytics · 2021Article
- Review
- Immunotherapeutic Efficacy of Retargeted oHSVs Designed for Propagation in an Ad Hoc Cell Line.Cancers · 2021Review
- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
- Herpes Simplex Virus Oncolytic Immunovirotherapy: The Blossoming Branch of Multimodal Therapy.International journal of molecular sciences · 2020Review
- Drug Conjugates for Targeting Eph Receptors in Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Point Mutations in Retargeted gD Eliminate the Sensitivity of EGFR/EGFRvIII-Targeted HSV to Key Neutralizing Antibodies.Molecular therapy. Methods & clinical development · 2020Article
- Anti-viral immunity in the tumor microenvironment: implications for the rational design of herpes simplex virus type 1 oncolytic virotherapy.Current clinical microbiology reports · 2019Article
- Review
- Oncolytic herpes simplex virus tumor targeting and neutralization escape by engineering viral envelope glycoproteins.Drug delivery · 2018Review
- Receptor-Targeted Glial Brain Tumor Therapies.International journal of molecular sciences · 2018Review
- Herpes Simplex Virus Vectors for Gene Transfer to the Central Nervous System.Diseases (Basel, Switzerland) · 2018Review
- HSV as A Platform for the Generation of Retargeted, Armed, and Reporter-Expressing Oncolytic Viruses.Viruses · 2018Article
- Dual Ligand Insertion in gB and gD of Oncolytic Herpes Simplex Viruses for Retargeting to a Producer Vero Cell Line and to Cancer Cells.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Current design of genetically engineered viruses for selective destruction of cancer cells is based on the observation that attenuated viruses replicate better in tumor cells than in normal cells. The ideal virus, however, is one that can infect only cancer cells by virtue of altered host range. Such a virus can be made more robust than the highly attenuated viruses used in clinical trials. Earlier, we reported the construction of a recombinant herpes simplex virus 1 (R5111) in which the capacity to bind heparan sulfate was disabled and which contained a chimeric IL-13-glycoprotein D that enabled the virus to infect cells expressing the IL-13alpha2 receptor (IL-13Ralpha2) commonly found on the surface of malignant glioblastomas or high-grade astrocytomas. In the earlier report, we showed that the recombinant R5111 was able to enter and infect cells via the interaction of the chimeric glycoprotein D with IL-13Ralpha2 but that the virus retained the capacity to bind and replicate in cells expressing the natural viral receptors HveA or nectin-1. Here, we report the construction of a recombinant virus (R5141) that can only enter and replicate in cells that express the IL-13Ralpha2. The recombinant R5141 does not depend on endocytosis to infect cells. It does not infect cells expressing HveA or nectin-1 receptors or cells expressing IL-13Ralpha2 that had been exposed to soluble IL-13 before infection. The studies described here show that the host range of herpes simplex viruses can be altered by genetic manipulation to specifically target cancer cells.
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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.