ArticleJournal of virology2003
Promoter sequences of varicella-zoster virus glycoprotein I targeted by cellular transactivating factors Sp1 and USF determine virulence in skin and T cells in SCIDhu mice in vivo.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Creating the "Dew Drop on a Rose Petal": the Molecular Pathogenesis of Varicella-Zoster Virus Skin Lesions.Microbiology and molecular biology reviews : MMBR · 2023Review
- Insights into the pathogenesis of varicella viruses.Current clinical microbiology reports · 2019Article
- Article
- Full trans-activation mediated by the immediate-early protein of equine herpesvirus 1 requires a consensus TATA box, but not its cognate binding sequence.Virus research · 2016Article
- Differential effects of Sp cellular transcription factors on viral promoter activation by varicella-zoster virus (VZV) IE62 protein.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
- An Sp1/Sp3 site in the downstream region of varicella-zoster virus (VZV) oriS influences origin-dependent DNA replication and flanking gene transcription and is important for VZV replication in vitro and in human skin.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
- Investigation of varicella-zoster virus neurotropism and neurovirulence using SCID mouse-human DRG xenografts.Journal of neurovirology · 2011Review
- Role of the IE62 consensus binding site in transactivation by the varicella-zoster virus IE62 protein.Journal of virology · 2010Article
- Regulation of the ORF61 promoter and ORF61 functions in varicella-zoster virus replication and pathogenesis.Journal of virology · 2009Article
- Deletion of the first cysteine-rich region of the varicella-zoster virus glycoprotein E ectodomain abolishes the gE and gI interaction and differentially affects cell-cell spread and viral entry.Journal of virology · 2009Article
- The phosphorylation profile of protein kinase A substrates is modulated during Varicella-zoster virus infection.Medical microbiology and immunology · 2008Article
- Cellular transcription factors Sp1 and Sp3 suppress varicella-zoster virus origin-dependent DNA replication.Journal of virology · 2008Article
- DNA vaccines: ready for prime time?Nature reviews. Genetics · 2008Review
- Cellular and viral factors regulate the varicella-zoster virus gE promoter during viral replication.Journal of virology · 2007Article
- Aberrant infection and persistence of varicella-zoster virus in human dorsal root ganglia in vivo in the absence of glycoprotein I.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The ubiquitous cellular transcriptional factor USF targets the varicella-zoster virus open reading frame 10 promoter and determines virulence in human skin xenografts in SCIDhu mice in vivo.Journal of virology · 2007Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Varicella-zoster virus (VZV) glycoprotein I is dispensable in cell culture but necessary for infection of human skin and T cells in SCIDhu mice in vivo. The gI promoter contains an activating upstream sequence that binds the cellular transactivators specificity factor 1 (Sp1) and upstream stimulatory factor (USF) and an open reading frame 29 (ORF29)-responsive element (29RE), which mediates enhancement by ORF29 DNA binding protein of immediate-early 62 (IE62)-induced transcription. Recombinants, rOKAgI-Sp1 and rOKAgI-USF, with two base pair substitutions in Sp1 or USF sites, replicated like rOKA in vitro, but infectivity of rOKAgI-Sp1 was significantly impaired in skin and T cells in vivo. A double mutant, rOKAgI-Sp1/USF, did not replicate in skin but yielded low titers of infectious virus in T cells. The repaired protein, rOKAgI:rep-Sp1/USF, was as infectious as rOKA. Thus, disrupting gI promoter sites for cellular transactivators altered VZV virulence in vivo, with variable consequences related to the cellular factor and the host cell type. Mutations in the 29RE of the gI promoter were made by substituting each of four 10-bp blocks in this region with a 10-bp sequence, GATAACTACA, that was predicted to interfere with enhancer effects of the ORF29 protein. One of these mutants, which was designated rOKAgI-29RE-3, had diminished replication in skin and T cells, indicating that ORF29 protein-mediated enhancement of gI expression contributes to VZV virulence. Mutations within promoters of viral genes that are nonessential in vitro should allow construction of recombinant herpesviruses that have altered virulence in specific host cells in vivo and may be useful for designing herpesviral gene therapy vectors and attenuated viral vaccines.
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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.