ArticleJournal of virology2002
Varicella-zoster virus (VZV) ORF17 protein induces RNA cleavage and is critical for replication of VZV at 37 degrees C but not 33 degrees C.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 44 citations in OpenAlex.
- Decoding VZV's evolutionary arsenal: how Beijing strains use recombination and adaptive mutations to thrive.Virus evolution · 2025Article
- Translational arrest and mRNA decay are independent activities of alphaherpesvirus virion host shutoff proteins.The Journal of general virology · 2024Article
- Article
- Host shutoff activity of VHS and SOX-like proteins: role in viral survival and immune evasion.Virology journal · 2020Review
- Review
- Going the Distance: Optimizing RNA-Seq Strategies for Transcriptomic Analysis of Complex Viral Genomes.Journal of virology · 2019Review
- Modeling Varicella Zoster Virus Persistence and Reactivation - Closer to Resolving a Perplexing Persistent State.Frontiers in microbiology · 2019Review
- Molecular characterization of duck enteritis virus UL41 protein.Virology journal · 2018Article
- Shutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common Themes.Viruses · 2016Review
- Review
- Neuronal changes induced by Varicella Zoster Virus in a rat model of postherpetic neuralgia.Virology · 2015Article
- Sequencing and characterization of Varicella-zoster virus vaccine strain SuduVax.Virology journal · 2011Article
- Genome-wide mutagenesis reveals that ORF7 is a novel VZV skin-tropic factor.PLoS pathogens · 2010Article
- Insulin degrading enzyme induces a conformational change in varicella-zoster virus gE, and enhances virus infectivity and stability.PloS one · 2010Article
- A varicella-zoster virus mutant impaired for latency in rodents, but not impaired for replication in cell culture.Virology · 2010Article
- The varicella-zoster virus genome.Current topics in microbiology and immunology · 2010Review
- Rodent models of varicella-zoster virus neurotropism.Current topics in microbiology and immunology · 2010Review
- Varicella-zoster virus open reading frame 66 protein kinase is required for efficient viral growth in primary human corneal stromal fibroblast cells.Journal of virology · 2008Article
- Downregulation of class I major histocompatibility complex surface expression by varicella-zoster virus involves open reading frame 66 protein kinase-dependent and -independent mechanisms.Journal of virology · 2007Article
- Inhibition of the NF-kappaB pathway by varicella-zoster virus in vitro and in human epidermal cells in vivo.Journal of virology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Varicella-zoster virus (VZV) open reading frame 17 (ORF17) is homologous to herpes simplex virus (HSV) UL41, which encodes the viral host shutoff protein (vhs). HSV vhs induces degradation of mRNA and rapid shutoff of host protein synthesis. An antibody to ORF17 protein detected a 46-kDa protein in VZV-infected cells. While HSV vhs is located in virions, VZV ORF17 protein was not detectable in virions. ORF17 protein induced RNA cleavage, but to a substantially lesser extent than HSV-1 vhs. Expression of ORF17 protein did not inhibit expression from a beta-galactosidase reporter plasmid, while HSV type 1 vhs abolished reporter expression. Two VZV ORF17 deletion mutants were constructed to examine the role of ORF17 in virus replication. While the ORF17 VZV mutants grew to peak titers that were similar to those of the parental virus at 33 degrees C, the ORF17 mutants grew to 20- to 35-fold-lower titers than parental virus at 37 degrees C. ORF62 protein was distributed in a different pattern in the nuclei and cytoplasm of cells infected with an ORF17 deletion mutant at 37 degrees C compared to 33 degrees C. Inoculation of cotton rats with the ORF17 deletion mutant resulted in a level of latent infection similar to that produced by inoculation with the parental virus. The importance of ORF17 protein for viral replication at 37 degrees C but not at 33 degrees C suggests that this protein may facilitate the growth of virus in certain tissues in vivo.
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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.