ArticleJournal of virology2012
Deletion of the herpes simplex virus 1 UL49 gene results in mRNA and protein translation defects that are complemented by secondary mutations in UL41.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Combinatorial genome engineering of pseudorabies virus Bartha by developing a reverse genetic system based on three overlapping genomic segments.Journal of advanced research · 2026Article
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
- Duck plague virus tegument protein vp22 plays a key role in the secondary envelopment and cell-to-cell spread.Veterinary research · 2023Article
- Dysregulated metabolism of the late herpes simplex virus 1 transcriptome through the vhs-VP22 axis uncouples virus cytopathic effect and virus production.PLoS pathogens · 2023Article
- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.Reviews in medical virology · 2022Review
- Article
- Herpes Simplex Virus 1 Expressing GFP-Tagged Virion Host Shutoff (vhs) Protein Uncouples the Activities of RNA Degradation and Differential Nuclear Retention of the Virus Transcriptome.Journal of virology · 2022Article
- Preventing translational inhibition from ribosomal protein insufficiency by a herpes simplex virus-encoded ribosome-associated protein.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Dissecting Herpes Simplex Virus 1-Induced Host Shutoff at the RNA Level.Journal of virology · 2021Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- Identification of a herpes simplex virus 1 gene encoding neurovirulence factor by chemical proteomics.Nature communications · 2020Article
- VHS, US3 and UL13 viral tegument proteins are required for Herpes Simplex Virus-Induced modification of protein kinase R.Scientific reports · 2020Article
- Alphaherpesvirus Major Tegument Protein VP22: Its Precise Function in the Viral Life Cycle.Frontiers in microbiology · 2020Review
- The herpes simplex virus host shutoff (vhs) RNase limits accumulation of double stranded RNA in infected cells: Evidence for accelerated decay of duplex RNA.PLoS pathogens · 2019Article
- Characteristics of herpes simplex virus infection and pathogenesis suggest a strategy for vaccine development.Reviews in medical virology · 2019Review
- Article
- Multiple Posttranscriptional Strategies To Regulate the Herpes Simplex Virus 1 vhs Endoribonuclease.Journal of virology · 2018Article
- Varicella-Zoster Virus ORF9p Binding to Cellular Adaptor Protein Complex 1 Is Important for Viral Infectivity.Journal of virology · 2018Article
- Decreased expression of the immediate early protein, ICP4, by deletion of the tegument protein VP22 of equine herpesvirus type 1.The Journal of veterinary medical science · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Herpes simplex virus 1 (HSV-1) virions, like those of all herpesviruses, contain a protein layer termed the tegument localized between the capsid and the envelope. VP22, encoded by the U(L)49 gene, is one of the most abundant tegument proteins in HSV-1 virions. Studies with a U(L)49-null mutant showed that the absence of VP22 resulted in decreased protein synthesis at late times in infection. VP22 is known to form a tripartite complex with VP16 and vhs through direct interactions with VP16. Given that U(L)49-null mutants have been shown to acquire spontaneous secondary mutations in the U(L)41 gene, which encodes vhs, we hypothesized that VP22 and vhs may play antagonistic roles during HSV-1 infections. In the present study, we show that the protein synthesis defect observed in U(L)49-null virus infections was rescued by a secondary, compensatory frameshift mutation in U(L)41. A double mutant bearing a deletion of U(L)49 and a point mutation in vhs previously shown to specifically abrogate vhs's RNase activity also resulted in a rescue of protein synthesis. To determine whether the U(L)49(-) protein synthesis defect, and the rescue by secondary mutations in vhs, occurred at the mRNA and/or translational levels, quantitative reverse transcriptase PCR (qRT-PCR) and polysome analyses were performed. We found that the absence of VP22 caused a small decrease in mRNA levels as well as a defect in polysome assembly that was independent of mRNA abundance. Both defects were complemented by the secondary mutations in vhs, indicating functional interplay between VP22 and vhs in both accumulation and translation of viral mRNAs.
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