Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Herpes simplex virus 1716, an ICP 34.5 null mutant, is unable to replicate in CV-1 cells due to a translational block that can be overcome by coinfection with SV40.

The Journal of general virology - 1 Dec 1997

Randazzo B P, Tal-Singer R, Zabolotny J M, Kesari S, Fraser N W

Abstract excerpt

Herpes simplex virus (HSV) mutants lacking the gene encoding infected cell protein (ICP) 34.5 exhibit an attenuated phenotype in models of pathogenesis and have been used for experimental cancer therapy. Recently it was shown that the HSV ICP 34.5 protein functions to prevent the host cell-induce...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Line
Share to Haplorhini
Share to Mutation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Protein Biosynthesis

Share to Simian virus 40

Share to Simplexvirus

Share to Viral Proteins

Share to Virus Replication

Source

Identifiers

PMID: 9400985
DOI: 10.1099/0022-1317-78-12-3333

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-9400985-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Herpes simplex virus 1716, an ICP 34.5 null mutant, is unable to replicate in CV-1 cells due to a translational block that can be overcome by coinfection with SV40.PMID 9400985Read ↗

Analysis of the Role of Autophagy in Replication of Herpes Simplex Virus in Cell CultureSemantic proximity Read ↗

The second-site mutation in the herpes simplex virus recombinants lacking the gamma134.5 genes precludes shutoff of protein synthesis by blocking the phosphorylation of eIF-2alpha.Semantic proximity Read ↗

In Vivo Replication of an ICP34.5 Second-Site Suppressor Mutant following Corneal Infection Correlates with In Vitro Regulation of eIF2α PhosphorylationSemantic proximity Read ↗

Amino acid substitution mutations in the herpes simplex virus ICP27 protein define an essential gene regulation function.Semantic proximity Read ↗

A conserved domain of herpes simplex virus ICP34.5 regulates protein phosphatase complex in mammalian cells.Semantic proximity Read ↗

Neurovirulent factor ICP34.5 uniquely expressed in the herpes simplex virus type 1 Delta gamma 1 34.5 mutant 1716.Semantic proximity Read ↗

The herpes simplex virus US11 protein effectively compensates for the gamma1(34.5) gene if present before activation of protein kinase R by precluding its phosphorylation and that of the alpha subunit of eukaryotic translation initiation factor 2.Semantic proximity Read ↗

ICP34.5 influences herpes simplex virus type 1 maturation and egress from infected cells in vitro.Semantic proximity Read ↗

A virus with a mutation in the ICP4-binding site in the L/ST promoter of herpes simplex virus type 1, but not a virus with a mutation in open reading frame P, exhibits cell-type-specific expression of gamma(1)34.5 transcripts and latency-associated transcripts.Semantic proximity Read ↗

Intracellular localization of the herpes simplex virus type 1 major transcriptional regulatory protein, ICP4, is affected by ICP27.Semantic proximity Read ↗

A herpesvirus genetic element which affects translation in the absence of the viral GADD34 function.Semantic proximity Read ↗

Replication of Herpes Simplex Virus 1 Depends on the γ <sub>1</sub> 34.5 Functions That Facilitate Virus Response to Interferon and Egress in the Different Stages of Productive InfectionSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.