ArticleJournal of virology1994
Varicella-zoster virus (VZV) open reading frame 10 protein, the homolog of the essential herpes simplex virus protein VP16, is dispensable for VZV replication in vitro.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 76 citations in OpenAlex.
- Non-neuronal sites of latency for alphaherpesviruses.Journal of virology · 2026Review
- Characterizing a newly identified avian herpesvirus-specific gene SORF3 in DPV and its roles in potential pathogenicity.Journal of virology · 2026Article
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Duck Plague Virus pUL48 Protein Activates the Immediate-Early Gene to Initiate the Transcription of the Virus Gene.Frontiers in microbiology · 2021Article
- The Role of VP16 in the Life Cycle of Alphaherpesviruses.Frontiers in microbiology · 2020Review
- Identification of non-essential loci within the Meleagrid herpesvirus 1 genome.Virology journal · 2015Article
- A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation.The Journal of general virology · 2015Review
- ORF9p phosphorylation by ORF47p is crucial for the formation and egress of varicella-zoster virus viral particles.Journal of virology · 2013Article
- Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.Journal of virology · 2012Article
- Herpes simplex virus and varicella zoster virus, the house guests who never leave.Herpesviridae · 2012Article
- Probing of the nuclear import and export signals and subcellular transport mechanism of varicella-zoster virus tegument protein open reading frame 10.Medical microbiology and immunology · 2012Article
- Analysis of the interaction between the essential herpes simplex virus 1 tegument proteins VP16 and VP1/2.Journal of virology · 2012Article
- Cloning the simian varicella virus genome in E. coli as an infectious bacterial artificial chromosome.Archives of virology · 2011Article
- Varicella zoster virus latency.Future virology · 2011Article
- Genome-wide mutagenesis reveals that ORF7 is a novel VZV skin-tropic factor.PLoS pathogens · 2010Article
- Improving the yeast two-hybrid system with permutated fusions proteins: the Varicella Zoster Virus interactome.Proteome science · 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
- Complete DNA sequences of two oka strain varicella-zoster virus genomes.Journal of virology · 2008Article
- Functions of the ORF9-to-ORF12 gene cluster in varicella-zoster virus replication and in the pathogenesis of skin infection.Journal of virology · 2008Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Varicella-zoster virus (VZV) open reading frame 10 (ORF10) protein in the homolog of the herpes simplex virus type 1 (HSV-1) protein VP16. VZV ORF10 transactivates the VZV IE62 gene and is a tegument protein present in the virion. HSV-1 VP16, a potent transactivator of HSV-1 immediate-early genes and tegument protein, is essential for HSV-1 replication in vitro. To determine whether VZV ORF10 is required for viral replication in vitro, we constructed two VZV mutants which were unable to express ORF10. One mutant had a stop codon after the 61st codon of the ORF10 gene, and the other mutant was deleted for all but the last five codons of the gene. Both VZV mutants grew in cell culture to titers similar to that of the parental virus. To determine whether HSV-1 VP16 alters the growth of VZV, we constructed a VZV mutant in which VP16 was inserted in place of ORF10. Using immune electron microscopy, we found that HSV-1 VP16 was present in the tegument of the recombinant VZV virions. The VZV VP16 substitution mutant produced smaller plaques and grew to a lower titer than parental virus. Thus, VZV ORF10 is not required for growth of the virus in vitro, and substitution of HSV-1 VP16 for VZV ORF10 impairs the growth of VZV.
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