ArticleJournal of virology2004
The varicella-zoster virus open reading frame 63 latency-associated protein is critical for establishment of latency.
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 39 papers.
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Who cites it
39 citing papers in PubMed.
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Deletion of Double Copies of the US1 Gene Reduces the Infectivity of Recombinant Duck Plague VirusMicrobiology spectrum · 2022Article
- Rapid Detection of the Varicella-Zoster Virus Using a Recombinase-Aided Amplification-Lateral Flow System.Diagnostics (Basel, Switzerland) · 2022Article
- Human herpesvirus diversity is altered in HLA class I binding peptides.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Varicella-zoster virus early infection but not complete replication is required for the induction of chronic hypersensitivity in rat models of postherpetic neuralgia.PLoS pathogens · 2021Article
- Multifaceted Roles of ICP22/ORF63 Proteins in the Life Cycle of Human Herpesviruses.Frontiers in microbiology · 2021Review
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
- Review
- Long-read sequencing uncovers a complex transcriptome topology in varicella zoster virus.BMC genomics · 2018Article
- Varicella-Zoster Virus ORF63 Protects Human Neuronal and Keratinocyte Cell Lines from Apoptosis and Changes Its Localization upon Apoptosis Induction.Journal of virology · 2018Article
- Herpes zoster and the search for an effective vaccine.Clinical and experimental immunology · 2017Review
- Neuronal changes induced by Varicella Zoster Virus in a rat model of postherpetic neuralgia.Virology · 2015Article
- Activation of H2AX and ATM in varicella-zoster virus (VZV)-infected cells is associated with expression of specific VZV genes.Virology · 2014Article
- Inhibition of Bim enhances replication of varicella-zoster virus and delays plaque formation in virus-infected cells.Journal of virology · 2014Article
- Characterization of synonymous codon usage bias in the pseudorabies virus US1 gene.Virologica Sinica · 2012Article
- Varicella-Zoster virus ORF12 protein triggers phosphorylation of ERK1/2 and inhibits apoptosis.Journal of virology · 2012Article
- A sequence within the varicella-zoster virus (VZV) OriS is a negative regulator of DNA replication and is bound by a protein complex containing the VZV ORF29 protein.Journal of virology · 2011Article
- Varicella zoster virus-induced pain and post-herpetic neuralgia in the human host and in rodent animal models.Journal of neurovirology · 2011Article
- Differentiated neuroblastoma cells provide a highly efficient model for studies of productive varicella-zoster virus infection of neuronal cells.Journal of virology · 2011Article
- Review: The neurobiology of varicella zoster virus infection.Neuropathology and applied neurobiology · 2011Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Varicella-zoster virus (VZV) expresses at least six viral transcripts during latency. One of these transcripts, derived from open reading frame 63 (ORF63), is one of the most abundant viral RNAs expressed during latency. The VZV ORF63 protein has been detected in human and experimentally infected rodent ganglia by several laboratories. We have deleted >90% of both copies of the ORF63 gene from the VZV genome. Animals inoculated with the ORF63 mutant virus had lower mean copy numbers of latent VZV genomes in the dorsal root ganglia 5 to 6 weeks after infection than animals inoculated with parental or rescued virus, and the frequency of latently infected animals was significantly lower in animals infected with the ORF63 mutant virus than in animals inoculated with parental or rescued virus. In contrast, the frequency of animals latently infected with viral mutants in other genes that are equally or more impaired for replication in vitro, compared with the ORF63 mutant, is similar to that of animals latently infected with parental VZV. Examination of dorsal root ganglia 3 days after infection showed high levels of VZV DNA in animals infected with either ORF63 mutant or parental virus; however, by days 6 and 10 after infection, the level of viral DNA in animals infected with the ORF63 mutant was significantly lower than that in animals infected with parental virus. Thus, ORF63 is not required for VZV to enter ganglia but is the first VZV gene shown to be critical for establishment of latency. Since the present vaccine can reactivate and cause shingles, a VZV vaccine based on the ORF63 mutant virus might be safer.
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