ArticleJournal of virology1997
Transcriptional targeting of herpes simplex virus for cell-specific replication.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 106 citations in OpenAlex.
- Understanding the interplay between oHSV and the host immune system: Implications for therapeutic oncolytic virus development.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Growth, Purification, and Titration of Oncolytic Herpes Simplex Virus.Journal of visualized experiments : JoVE · 2021Article
- The discovery and development of oncolytic viruses: are they the future of cancer immunotherapy?Expert opinion on drug discovery · 2021Review
- A novel oHSV-1 targeting telomerase reverse transcriptase-positive cancer cells via tumor-specific promoters regulating the expression of ICP4.Oncotarget · 2015Article
- Review
- Oncolytic virotherapy using herpes simplex virus: how far have we come?Oncolytic virotherapy · 2015Review
- MicroRNA-145 regulates oncolytic herpes simplex virus-1 for selective killing of human non-small cell lung cancer cells.Virology journal · 2013Article
- Antiglioma oncolytic virotherapy: unattainable goal or a success story in the making?Future virology · 2013Article
- Oncolytic virotherapy.Nature biotechnology · 2012Review
- Development of an oncolytic herpes simplex virus using a tumor-specific HIF-responsive promoter.Cancer gene therapy · 2011Article
- Development of a regulatable oncolytic herpes simplex virus type 1 recombinant virus for tumor therapy.Journal of virology · 2010Article
- HSV Recombinant Vectors for Gene Therapy.The open virology journal · 2010Article
- Gene therapy: the end of the rainbow?Head & neck oncology · 2009Review
- An oncolytic mutant of herpes simplex virus type-1 in which replication is governed by a promoter/enhancer of human papillomavirus type-16.Cancer gene therapy · 2007Article
- Herpes simplex virus 1 (HSV-1) for cancer treatment.Cancer gene therapy · 2006Review
- Flip-Flop HSV-BAC: bacterial artificial chromosome based system for rapid generation of recombinant herpes simplex virus vectors using two independent site-specific recombinases.BMC biotechnology · 2006Article
- Replication-competent herpes simplex vectors: design and applications.Gene therapy · 2005Review
- Replication-selective oncolytic viruses in the treatment of cancer.Cancer gene therapy · 2005Review
- Herpes simplex virus-induced, death receptor-dependent apoptosis and regression of transplanted human cancers.Cancer science · 2004Article
- Oncolytic viral therapies.Cancer gene therapy · 2004Review
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 1 country.
Funding
Abstract
Tissue- or cell-specific targeting of vectors is critical to the success of gene therapy. We describe a novel approach to virus-mediated gene therapy, where viral replication and associated cytotoxicity are limited to a specific cell type by the regulated expression of an essential immediate-early viral gene product. This is illustrated with a herpes simplex virus type 1 (HSV-1) vector (G92A) whose growth is restricted to albumin-expressing cells. G92A was constructed by inserting an albumin enhancer/promoter-ICP4 transgene into the thymidine kinase gene of mutant HSV-1 d120, deleted for both copies of the ICP4 gene. This vector also contains the Escherichia coli lacZ gene under control of the thymidine kinase promoter, a viral early promoter, to permit easy detection of infected cells containing replicating vector. In the adult, albumin is expressed uniquely in the liver and in hepatocellular carcinoma and is transcriptionally regulated. The plaquing efficiency of G92A is > 10(3) times higher on human hepatoma cells than on non-albumin-expressing human cells. The growth kinetics of G92A in albumin-expressing cells is delayed compared with that of wild-type HSV-1, likely due to aberrant expression of ICP4 protein. Cells undergoing a productive infection expressed detectable levels of ICP4 protein, as well as the reporter gene product beta-galactosidase. Confining a productive, cytotoxic viral infection to a specific cell type should be useful for tumor therapy and the ablation of specific cell types for the generation of animal models of disease.
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What OpenQuestion holds
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.