ArticleJournal of virology2004
Role of the VP16-binding domain of vhs in viral growth, host shutoff activity, and pathogenesis.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Translational arrest and mRNA decay are independent activities of alphaherpesvirus virion host shutoff proteins.The Journal of general virology · 2024Article
- Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.Reviews in medical virology · 2022Review
- The Role of VP16 in the Life Cycle of Alphaherpesviruses.Frontiers in microbiology · 2020Review
- CD28 Costimulation Is Required for Development of Herpetic Stromal Keratitis but Does Not Prevent Establishment of Latency.Journal of virology · 2019Article
- The US11 Gene of Herpes Simplex Virus 1 Promotes Neuroinvasion and Periocular Replication following Corneal Infection.Journal of virology · 2019Article
- Attenuated Herpes Simplex Virus 1 (HSV-1) Expressing a Mutant Form of ICP6 Stimulates a Strong Immune Response That Protects Mice against HSV-1-Induced Corneal Disease.Journal of virology · 2018Article
- Generation and characterization of UL41 null pseudorabies virus variant in vitro and in vivo.Virology journal · 2018Article
- A bimodal switch in global protein translation coupled to eIF4H relocalisation during advancing cell-cell transmission of herpes simplex virus.PLoS pathogens · 2018Article
- Impaired Fas-Fas Ligand Interactions Result in Greater Recurrent Herpetic Stromal Keratitis in Mice.Journal of immunology research · 2015Article
- Herpes simplex virus 1 ICP22 but not US 1.5 is required for efficient acute replication in mice and VICE domain formation.Journal of virology · 2013Article
- mRNA decay during herpes simplex virus (HSV) infections: mutations that affect translation of an mRNA influence the sites at which it is cleaved by the HSV virion host shutoff (Vhs) protein.Journal of virology · 2013Article
- The virion host shutoff protein of herpes simplex virus 1 blocks the replication-independent activation of NF-κB in dendritic cells in the absence of type I interferon signaling.Journal of virology · 2011Article
- Herpes simplex virus 1 ICP0 phosphorylation site mutants are attenuated for viral replication and impaired for explant-induced reactivation.Journal of virology · 2011Article
- Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivo.Journal of neurovirology · 2010Article
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- Interaction of ICP34.5 with Beclin 1 modulates herpes simplex virus type 1 pathogenesis through control of CD4+ T-cell responses.Journal of virology · 2009Article
- Type I IFN response to Papiine herpesvirus 2 (Herpesvirus papio 2; HVP2) determines neuropathogenicity in mice.Virology · 2009Article
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- Small interfering RNAs that deplete the cellular translation factor eIF4H impede mRNA degradation by the virion host shutoff protein of herpes simplex virus.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The virion host shutoff (vhs) protein of herpes simplex virus type 1 causes the degradation of host and viral mRNA immediately upon infection of permissive cells. vhs can interact with VP16 through a 20-amino-acid binding domain, and viruses containing a deletion of this VP16-binding domain of vhs (Delta20) and a corresponding marker rescue (Delta20R) were constructed and characterized. Transient-transfection assays showed that this domain was dispensable for vhs activity. The Delta20 recombinant virus, however, was unable to induce mRNA degradation in the presence of actinomycin D, while degradation induced by Delta20R was equivalent to that for wild-type virus. Delta20, Delta20R, and KOS caused comparable RNA degradation in the absence of actinomycin D. Western blot analysis of infected cells indicated that comparable levels of vhs were expressed by Delta20, Delta20R, and KOS, and there was only a modest reduction of vhs packaging in Delta20. Immunoprecipitation of protein from cells infected with Delta20 and Delta20R showed equivalent coprecipitation of vhs and VP16. Pathogenesis studies with Delta20 showed a significant decrease in replication in the corneas, trigeminal ganglia, and brains, as well as a significant reduction in clinical disease and lethality, but no significant difference in the establishment of, or reactivation from, latency compared to results with KOS and Delta20R. These results suggest that the previously described VP16-binding domain is not required for vhs packaging or for binding to VP16. It is required, however, for RNA degradation activity of tegument-derived vhs and wild-type replication and virulence in mice.
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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.