ArticleGene therapy2008
A strategy for systemic delivery of the oncolytic herpes virus HSV1716: redirected tropism by antibody-binding sites incorporated on the virion surface as a glycoprotein D fusion protein.
Article in Gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Oncolytic viruses as cancer therapeutics: From mechanistic insights to clinical translation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Emerging delivery strategy for oncolytic virotherapy.Molecular therapy. Oncology · 2024Review
- Article
- The Dilemma of HSV-1 Oncolytic Virus Delivery: The Method Choice and Hurdles.International journal of molecular sciences · 2023Review
- Inconsistencies in Modeling the Efficacy of the Oncolytic Virus HSV1716 Reveal Potential Predictive Biomarkers for Tolerability.Frontiers in molecular biosciences · 2022Article
- Identification of 22 Novel Motifs of the Cell Entry Fusion Glycoprotein B of Oncolytic Herpes Simplex Viruses: Sequence Analysis and Literature Review.Frontiers in oncology · 2020Article
- Immunotherapeutic Challenges for Pediatric Cancers.Molecular therapy oncolytics · 2019Review
- Review
- High Mobility Group Box 1 Influences HSV1716 Spread and Acts as an Adjuvant to Chemotherapy.Viruses · 2018Article
- Immune Checkpoint Inhibition for Pancreatic Ductal Adenocarcinoma: Current Limitations and Future Options.Frontiers in immunology · 2018Review
- Construction of Various γ34.5 Deleted Fluorescent-Expressing Oncolytic herpes Simplex type 1 (oHSV) for Generation and Isolation of HSV-Based VectorsIranian biomedical journal · 2017Article
- Oncolytic Viruses-Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer.Frontiers in oncology · 2017Review
- Retargeting of herpes simplex virus (HSV) vectors.Current opinion in virology · 2016Review
- Oncolytic virotherapy for urological cancers.Nature reviews. Urology · 2016Review
- Pancreatic cancer from bench to bedside: molecular pathways and treatment options.Annals of translational medicine · 2016Review
- Viro-immune therapy: A new strategy for treatment of pancreatic cancer.World journal of gastroenterology · 2016Review
- Oncolytic virotherapy using herpes simplex virus: how far have we come?Oncolytic virotherapy · 2015Review
- Potent efficacy signals from systemically administered oncolytic herpes simplex virus (HSV1716) in hepatocellular carcinoma xenograft models.Journal of hepatocellular carcinoma · 2014Article
- Expression of inhibitor of growth 4 by HSV1716 improves oncolytic potency and enhances efficacy.Cancer gene therapy · 2012Article
- Oncolytic HSV-1 virotherapy: clinical experience and opportunities for progress.Current pharmaceutical biotechnology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report on the ability of single-chain variable fragment (scFv) incorporated into the viral envelope to alter the tropism of herpes simplex virus (HSV) 1716. Using recombinant viruses expressing fusion proteins comprising cell-surface antigen-specific scFvs N terminus linked to amino acids 274-393 of gD, we demonstrated that the tropism of these HSV1716 variants was modified such that infection was mediated by the cognate antigen. Thus, an HSV1716 variant that expressed an anti-CD55 scFv targeting moiety linked to these gD residues was able to infect non-permissive Chinese hamster ovary cells expressing CD55 and this infection was specifically blocked by an anti-CD55 monoclonal antibody. Similarly, the infection efficiency of an HSV1716 variant for semi-permissive human leukaemic, CD38-positive cell lines was greatly improved by an anti-CD38 scFv targeting moiety linked to gD residues 274-393, and this enhanced infectivity was abrogated specifically by an anti-CD38 monoclonal antibody. Finally, intravenous/intraperitoneal injection of an HSV1716 variant displaying an anti-epidermal growth factor receptor (EGFR) scFv linked to residues 274-393 of gD enhanced destruction of subcutaneous EGFR-positive tumours in nude mice compared to unmodified HSV1716. Therefore, targeting of HSV1716 oncolysis to specific cell types through the display of entry mediating scFv/gD fusion proteins represents an efficient route for systemic delivery.
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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.