ArticleJournal of virology2002
Role of the varicella-zoster virus gB cytoplasmic domain in gB transport and viral egress.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
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- Targeted mutagenesis of the herpesvirus fusogen central helix captures transition states.Nature communications · 2023Article
- The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
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- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
- Varicella-zoster virus: molecular controls of cell fusion-dependent pathogenesis.Biochemical Society transactions · 2020Review
- Calcineurin phosphatase activity regulates Varicella-Zoster Virus induced cell-cell fusion.PLoS pathogens · 2020Article
- Epstein-Barr Virus Fusion with Epithelial Cells Triggered by gB Is Restricted by a gL Glycosylation Site.Journal of virology · 2017Article
- The Glycoprotein B Cytoplasmic Domain Lysine Cluster Is Critical for Varicella-Zoster Virus Cell-Cell Fusion Regulation and Infection.Journal of virology · 2017Article
- Dysregulated Glycoprotein B-Mediated Cell-Cell Fusion Disrupts Varicella-Zoster Virus and Host Gene Transcription during Infection.Journal of virology · 2017Article
- Varicella-Zoster Virus Glycoproteins: Entry, Replication, and Pathogenesis.Current clinical microbiology reports · 2016Article
- Herpesvirus gB: A Finely Tuned Fusion Machine.Viruses · 2015Review
- An immunoreceptor tyrosine-based inhibition motif in varicella-zoster virus glycoprotein B regulates cell fusion and skin pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Optimal replication of human cytomegalovirus correlates with endocytosis of glycoprotein gpUL132.Journal of virology · 2010Article
- Mutagenesis of varicella-zoster virus glycoprotein B: putative fusion loop residues are essential for viral replication, and the furin cleavage motif contributes to pathogenesis in skin tissue in vivo.Journal of virology · 2009Article
- Primary B-cell infection with a deltaBALF4 Epstein-Barr virus comes to a halt in the endosomal compartment yet still elicits a potent CD4-positive cytotoxic T-cell response.Journal of virology · 2009Article
- Analysis of Epstein-Barr virus glycoprotein B functional domains via linker insertion mutagenesis.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To study the function of the varicella-zoster virus (VZV) gB cytoplasmic domain during viral infection, we produced a VZV recombinant virus that expresses a truncated form of gB lacking the C-terminal 36 amino acids of its cytoplasmic domain (VZV gB-36). VZV gB-36 replicates in noncomplementing cells and grows at a rate similar to that of native VZV. However, cells infected with VZVgB-36 form extensive syncytia compared to the relatively small syncytia formed during native VZV infection. In addition, electron microscopy shows that very little virus is present on the surfaces of cells infected with VZV gB-36, while cells infected with native VZV exhibit abundant virions on the cell surface. The C-terminal 36 amino acids of the gB cytoplasmic domain have been shown in transfection-based experiments to contain both an endoplasmic reticulum-to-Golgi transport signal (the C-terminal 17 amino acids) and a consensus YXXphi (where Y is tyrosine, X is any amino acid, and phi is any bulky hydrophobic amino acid) signal sequence (YSRV) that mediates the internalization of gB from the plasma membrane. As predicted based on these data, gB-36 expressed during the infection of cultured cells is transported inefficiently to the Golgi. Despite lacking the YSRV signal sequence, gB-36 is internalized from the plasma membrane; however, in contrast to native gB, it fails to localize to the Golgi. Therefore, the C-terminal 36 amino acids of the VZV gB cytoplasmic domain are required for normal viral egress and for both the pre- and post-Golgi transport of gB.
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