Evidence map›Paper›PMID 1373198›Full record

ArticleJournal of virology1992

Cytotoxicity of a replication-defective mutant of herpes simplex virus type 1.

P A Johnson, A Miyanohara, F Levine, T Cahill, T Friedmann

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
31.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 295 citations in OpenAlex.

  1. Review
  2. Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Gene delivery with viral vectors for cerebrovascular diseases.Frontiers in bioscience (Elite edition) · 2013
    Review
  12. Recognition of virus infection and innate host responses to viral gene therapy vectors.Molecular therapy : the journal of the American Society of Gene Therapy · 2010
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

P A JohnsonDepartment of Pediatrics, University of California, San Diego, La Jolla 92093-0634.
A Miyanohara
F Levine
T Cahill
T Friedmann
University of California San Diego · US

Funding

GENE EXPRESSION FROM RETROVIRAL VECTORS AND GENE THERAPYF32GM013538 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI LEVINE, FRED · 1989 to 1991
–
MODELS FOR CNS GENE THERAPYR01HD020034 · NICHD · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI FRIEDMANN, THEODORE · 1985 to 1994
–
NICHD NIH HHS CHD 20034NIGMS NIH HHS GM 13538
6 · The paper itself

Abstract

Replication-defective mutants of herpes simplex virus type 1 (HSV-1) may prove useful as vectors for gene transfer, particularly to nondividing cells. Cgal delta 3 is an immediate-early gene 3 (IE 3) deletion mutant of HSV-1 that expresses the lacZ gene of Escherichia coli from the human cytomegalovirus immediate-early control region but does not express viral early or late genes. This vector was able to efficiently infect and express lacZ in cells refractory to traditional methods of gene transfer. However, 1 to 3 days postinfection, Cgal delta 3 induced cytopathic effects (CPE) in many cell types, including neurons. In human primary fibroblasts Cgal delta 3 induced chromosomal aberrations and host cell DNA fragmentation. Other HSV-1 strains that caused CPE, tested under conditions of viral replication-inhibition, included mutants of the early gene UL42, the virion host shutoff function, single mutants of IE 1, IE 2, and IE 3, and double mutants of IE 3 and 4 and IE 3 and 5. Inhibition of viral gene expression by UV irradiation of virus stocks or by preexposure of cells to interferon markedly reduced the CPE. We conclude from these studies that HSV-1 IE gene expression is sufficient for the induction of CPE, although none of the five IE gene products appear to be solely responsible. After infection of human fibroblasts with Cgal delta 3 at a low multiplicity of infection, we were able to recover up to 6% of the input virus 2 weeks later by a superinfection-rescue procedure, even though the virally transduced human cytomegalovirus-lacZ transgene was not expressed at this time. It is therefore likely that inhibition or inactivation of viral IE gene expression, either for establishing latency or for the long-term transduction of foreign genes by HSV-1 vectors, is essential to avoid the death of infected cells.

Indexed as

Genetic VectorsHost-Parasite InteractionsVirus ReplicationAnimalsCell DeathChromosome AberrationsCytomegalovirusDNA DamageDNA, RecombinantEscherichia coliEvaluation Studies as TopicFibroblastsGene Expression Regulation, ViralHerpes SimplexHumansInterferonsDNA, RecombinantInterferons

Identifiers

PMID1373198
PMCPMC241054
OpenAlexW2116460986

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.