ArticleJournal of virology2008
Construction of a fully retargeted herpes simplex virus 1 recombinant capable of entering cells solely via human epidermal growth factor receptor 2.
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 78 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.
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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
78 citing papers in PubMed, 106 citations in OpenAlex.
- Engineering HSV-1 for oncolytic therapy: From molecular entry mechanisms to retargeting strategies.Genes & diseases · 2026Review
- Shaping viral immunotherapy towards cancer-targeted immunological cell death.Frontiers in oncology · 2025Review
- Challenges and strategies toward oncolytic virotherapy for leptomeningeal metastasis.Journal of translational medicine · 2024Review
- Integrating system biology and intratumor gene therapy by trans-complementing the appropriate co-stimulatory molecule as payload in oncolytic herpes virus.Cancer gene therapy · 2024Article
- Oncolytic herpes simplex viruses designed for targeted treatment of EGFR-bearing tumors.Molecular therapy. Oncology · 2024Article
- Article
- Tumor Tropism of DNA Viruses for Oncolytic Virotherapy.Viruses · 2023Review
- Novel mutations in UMolecular therapy. Methods & clinical development · 2023Article
- Article
- Oncolytic herpes simplex viruses for the treatment of glioma and targeting glioblastoma stem-like cells.Frontiers in cellular and infection microbiology · 2023Review
- Development and application of oncolytic viruses as the nemesis of tumor cells.Frontiers in microbiology · 2023Review
- Innovative retargeted oncolytic herpesvirus against nectin4-positive cancers.Frontiers in molecular biosciences · 2023Article
- Review
- Progress of oncolytic virotherapy for neuroblastoma.Frontiers in pediatrics · 2022Review
- Herpes simplex virus 1 as an oncolytic viral therapy for refractory cancers.Frontiers in oncology · 2022Review
- Generation of a Retargeted OncolyticInternational journal of molecular sciences · 2021Article
- Towards a Precision Medicine Approach and In Situ Vaccination against Prostate Cancer by PSMA-Retargeted oHSV.Viruses · 2021Article
- Article
- Viroimmunotherapy for breast cancer: promises, problems and future directions.Cancer gene therapy · 2021Review
- Oncolytic HSV: Underpinnings of Tumor Susceptibility.Viruses · 2021Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A novel frontier in the treatment of tumors that are difficult to treat is oncolytic virotherapy, in which a replication-competent virus selectively infects and destroys tumor cells. Herpes simplex virus (HSV) represents a particularly attractive system. Effective retargeting to tumor-specific receptors has been achieved by insertion in gD of heterologous ligands. Previously, our laboratory generated an HSV retargeted to human epidermal growth factor receptor 2 (HER2), a receptor overexpressed in about one-third of mammary tumors and in some ovarian tumors. HER2 overexpression correlates with increased metastaticity and poor prognosis. Because HER2 has no natural ligand, the inserted ligand was a single-chain antibody to HER2. The objective of this work was to genetically engineer an HSV that selectively targets the HER2-expressing tumor cells and that has lost the ability to enter cells through the natural gD receptors, HVEM and nectin1. Detargeting from nectin1 was attempted by two different strategies, point mutations and insertion of the single-chain antibody at a site in gD different from previously described sites of insertion. We report that point mutations at gD amino acids 34, 215, 222, and 223 failed to generate a nectin1-detargeted HSV. An HSV simultaneously detargeted from nectin1 and HVEM and retargeted to HER2 was successfully engineered by moving the site of single-chain antibody insertion at residue 39, i.e., in front of the nectin1-interacting surface and not lateral to it, and by deleting amino acid residues 6 to 38. The resulting recombinant, R-LM113, entered cells and spread from cell to cell solely via HER2.
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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.