ArticleJournal of virology1997
Varicella-zoster virus glycoprotein I is essential for growth of virus in Vero cells.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 66 citations in OpenAlex.
- The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
- Article
- Interferon Inhibition Enhances the Pilot-Scale Production of Rabies Virus in Human Diploid MRC-5 Cells.Viruses · 2021Article
- Viral cell-to-cell spread: Conventional and non-conventional ways.Advances in virus research · 2020Review
- Activation of H2AX and ATM in varicella-zoster virus (VZV)-infected cells is associated with expression of specific VZV genes.Virology · 2014Article
- Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.Journal of virology · 2012Article
- Functions of the unique N-terminal region of glycoprotein E in the pathogenesis of varicella-zoster virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The varicella-zoster virus genome.Current topics in microbiology and immunology · 2010Review
- Article
- Quantitative measurement of varicella-zoster virus infection by semiautomated flow cytometry.Applied and environmental microbiology · 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
- Avoiding the void: cell-to-cell spread of human viruses.Nature reviews. Microbiology · 2008Review
- Varicella-zoster virus open reading frame 66 protein kinase is required for efficient viral growth in primary human corneal stromal fibroblast cells.Journal of virology · 2008Article
- A self-excisable infectious bacterial artificial chromosome clone of varicella-zoster virus allows analysis of the essential tegument protein encoded by ORF9.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
- Varicella-Zoster virus IE63, a major viral latency protein, is required to inhibit the alpha interferon-induced antiviral response.Journal of virology · 2007Article
- The amino terminus of varicella-zoster virus (VZV) glycoprotein E is required for binding to insulin-degrading enzyme, a VZV receptor.Journal of virology · 2007Article
- Article
- Essential functions of the unique N-terminal region of the varicella-zoster virus glycoprotein E ectodomain in viral replication and in the pathogenesis of skin infection.Journal of virology · 2006Article
- Comparison of virus transcription during lytic infection of the Oka parental and vaccine strains of Varicella-Zoster virus.Journal of virology · 2006Article
Corrections and comments
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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) encodes at least six glycoproteins. Glycoprotein I (gI), the product of open reading frame 67, is a 58- to 62-kDa glycoprotein found in VZV-infected cells. We constructed two VZV gI deletion mutants. Immunoprecipitation of VZV gE from infected cells indicated that cells infected with VZV deleted for gI expressed a gE that was larger (100 kDa) than that expressed in cells infected with the parental virus (98 kDa). Cell-associated or cell-free VZV deleted for gI grew to lower titers in melanoma cells than did parental VZV. While VZV deleted for gI replicated in other human cells, the mutant virus replicated to very low titers in primary guinea pig and monkey cells and did not replicate in Vero cells. When compared with the parental virus, rescued viruses, in which the gI deletion was restored with a wild-type allele, showed a similarly sized gE and comparable growth patterns in melanoma and Vero cells. VZV deleted for gI entered Vero cells; however, viral DNA synthesis was impaired in these cells. The VZV gI mutant was slightly impaired for adsorption to human cells. Thus, VZV gI is required for replication of the virus in Vero cells, for efficient replication of the virus in nonhuman cells, and for normal processing of gE.
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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.