ArticleJournal of virology2009
Regulation of the ORF61 promoter and ORF61 functions in varicella-zoster virus replication and pathogenesis.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 37 citations in OpenAlex.
- Identification and characterization of Varicella Zoster Virus circular RNA in lytic infection.Nature communications · 2024Article
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Shaping the host cell environment with viral noncoding RNAs.Seminars in cell & developmental biology · 2023Review
- Varicella-Zoster Virus-Genetics, Molecular Evolution and Recombination.Current topics in microbiology and immunology · 2023Article
- G-quadruplexes formed by Varicella-Zoster virus reiteration sequences suppress expression of glycoprotein C and regulate viral cell-to-cell spread.PLoS pathogens · 2023Article
- Simian Varicella Virus: Molecular Virology and Mechanisms of Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Insights From Studies of the Genetics, Pathogenesis, and Immunogenicity of the Varicella Vaccine.The Journal of infectious diseases · 2022Article
- Article
- Molecular Aspects of Varicella-Zoster Virus Latency.Viruses · 2018Review
- A spliced latency-associated VZV transcript maps antisense to the viral transactivator gene 61.Nature communications · 2018Article
- Dysregulated Glycoprotein B-Mediated Cell-Cell Fusion Disrupts Varicella-Zoster Virus and Host Gene Transcription during Infection.Journal of virology · 2017Article
- Differential effects of Sp cellular transcription factors on viral promoter activation by varicella-zoster virus (VZV) IE62 protein.Virology · 2015Article
- The ORF61 Protein Encoded by Simian Varicella Virus and Varicella-Zoster Virus Inhibits NF-κB Signaling by Interfering with IκBα Degradation.Journal of virology · 2015Article
- Molecular mechanisms of varicella zoster virus pathogenesis.Nature reviews. Microbiology · 2014Review
- Cellular transcription factor YY1 mediates the varicella-zoster virus (VZV) IE62 transcriptional activation.Virology · 2014Article
- Regulation of the varicella-zoster virus ORF3 promoter by cellular and viral factors.Virology · 2013Article
- Identification of a hydrophobic domain in varicella-zoster virus ORF61 necessary for ORF61 self-interaction, viral replication, and skin pathogenesis.Journal of virology · 2013Article
- Attenuation of the adaptive immune response in rhesus macaques infected with simian varicella virus lacking open reading frame 61.Journal of virology · 2013Article
- Varicella-zoster virus inhibition of the NF-κB pathway during infection of human dendritic cells: role for open reading frame 61 as a modulator of NF-κB activity.Journal of virology · 2012Article
- Disruption of PML nuclear bodies is mediated by ORF61 SUMO-interacting motifs and required for varicella-zoster virus pathogenesis in skin.PLoS pathogens · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Varicella-zoster virus (VZV) open reading frame 61 (ORF61) encodes a protein that transactivates viral and cellular promoters in transient-transfection assays and is the ortholog of herpes simplex virus ICP0. In this report, we mapped the ORF61 promoter and investigated its regulation by viral and cellular proteins in transient-expression experiments and by mutagenesis of the VZV genome (parent Oka strain). The 5' boundary of the minimal ORF61 promoter required for IE62 transactivation was mapped to position -95 relative to the mRNA start site, and three noncanonical GT-rich Sp1-binding sites were documented to occur within the region comprising positions -95 to -45. Contributions of the three Sp1-binding-site motifs, designated Sp1a, Sp1b, and Sp1c, to ORF61 expression and viral replication were varied despite their similar sequences. Two sites, Sp1a and Sp1c, functioned synergistically. When both sites were mutated in the pOka genome to produce pOka-61proDeltaSp1ac, the mutant virus expressed significantly less ORF61 protein. Using this mutant to investigate ORF61 functions resulted in reductions in the expression levels of IE proteins, viral kinases ORF47 and ORF66, and the major glycoprotein gE, with the most impact on gE. Virion morphogenesis appeared to be intact despite minimal ORF61 expression. Pretreating melanoma cells with sodium butyrate enhanced titers of pOka-61proDeltaSp1ac but not pOka, suggesting that ORF61 has a role in histone deacetylase inhibition. Growth of pOka-61proDeltaSp1ac was impaired in SCIDhu skin xenografts, indicating that the regulation of the ORF61 promoter by Sp1 family proteins is important for ORF61 expression in vivo and that ORF61 contributes to VZV virulence at skin sites of replication.
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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.