ArticleVirology2011
Identification and functional characterization of the Varicella zoster virus ORF11 gene product.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 13 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
- The Tegument Protein pUL47 of Marek's Disease Virus Is Necessary for Horizontal Transmission and Is Important for Expression of Glycoprotein gC.Journal of virology · 2020Article
- Article
- Increase in the genetic polymorphism of varicella-zoster virus after passaging in in vitro cell culture.Journal of microbiology (Seoul, Korea) · 2019Article
- Varicella zoster virus infection of human fetal lung cells alters mitochondrial morphology.Journal of neurovirology · 2016Article
- Evolution of cocirculating varicella-zoster virus genotypes during a chickenpox outbreak in Guinea-Bissau.Journal of virology · 2014Article
- ORF11 protein interacts with the ORF9 essential tegument protein in varicella-zoster virus infection.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The deletion of ORF11 severely impaired VZV infection of human skin xenografts. Here, we investigate the characteristics and functions of the ORF11 gene product. ORF11 is expressed as a 118kDa polypeptide in VZV-infected cells; the protein is present in the nucleus and cytoplasm and is incorporated into VZ virions. Although ORF11 had little effect in transactivating VZV gene promoters in transfection assays, deleting ORF11 from the virus was associated with reduced expression of immediate early proteins IE4, IE62 and IE63, and the major glycoprotein, gE. ORF11 was identified as an RNA binding protein and its RNA binding domain was defined. However, disrupting the ORF11 RNA binding domain did not affect skin infection, indicating that RNA binding capacity, conserved among the alphaherpesviruses homologues, is not essential while the contribution of ORF11 to the expression of the IE proteins and gE may be required for VZV pathogenesis in skin in vivo.
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Registered trials
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