ArticleJournal of virology2009
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.
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 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Comparative Antibody Responses to the Live-Attenuated and Recombinant Herpes Zoster Vaccines.Journal of virology · 2021Trial
- Microglial MARCO facilitates Varicella zoster virus uptake and triggers TLR2-mediated neuroinflammation.Journal of biomedical science · 2026Article
- A novel replication-deficient feline herpesvirus type 1 vector-based vaccine provides strong immune protection in cats.Journal of virology · 2026Article
- Immunogenicity and cellular response of a herpes zoster virus gEgI fusion protein adjuvanted with CpG-emulsion in mice.Journal of nanobiotechnology · 2025Article
- Exploring viral neuropathic pain: Molecular mechanisms and therapeutic implications.PLoS pathogens · 2024Review
- 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 Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
- Novel BC02 Compound Adjuvant Enhances Adaptive and Innate Immunity Induced by Recombinant Glycoprotein E of Varicella-Zoster Virus.Vaccines · 2022Article
- Evaluation of safety and immunogenicity of duck-plague virus gC/gE double gene deletion.Frontiers in immunology · 2022Article
- Review
- Evaluation of the Safety and Immunogenicity of Duck-Plague VirusFrontiers in immunology · 2022Article
- The N-terminus of varicella-zoster virus glycoprotein B has a functional role in fusion.PLoS pathogens · 2021Article
- Varicella-zoster virus: molecular controls of cell fusion-dependent pathogenesis.Biochemical Society transactions · 2020Review
- Article
- Varicella Virus-Host Interactions During Latency and Reactivation: Lessons From Simian Varicella Virus.Frontiers in microbiology · 2018Review
- 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
- Global Mapping of O-Glycosylation of Varicella Zoster Virus, Human Cytomegalovirus, and Epstein-Barr Virus.The Journal of biological chemistry · 2016Article
- Immunogenicity of varicella zoster virus glycoprotein E DNA vaccine.Experimental and therapeutic medicine · 2016Article
- Sialic Acids on Varicella-Zoster Virus Glycoprotein B Are Required for Cell-Cell Fusion.The Journal of biological chemistry · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Varicella-zoster virus (VZV) glycoprotein E (gE) is the most abundant glycoprotein in infected cells and, in contrast to those of other alphaherpesviruses, is essential for viral replication. The gE ectodomain contains a unique N-terminal region required for viral replication, cell-cell spread, and secondary envelopment; this region also binds to the insulin-degrading enzyme (IDE), a proposed VZV receptor. To identify new functional domains of the gE ectodomain, the effect of mutagenesis of the first cysteine-rich region of the gE ectodomain (amino acids 208 to 236) was assessed using VZV cosmids. Deletion of this region was compatible with VZV replication in vitro, but cell-cell spread of the rOka-DeltaCys mutant was reduced significantly. Deletion of the cysteine-rich region abolished the binding of the mutant gE to gI but not to IDE. Preventing gE binding to gI altered the pattern of gE expression at the plasma membrane of infected cells and the posttranslational maturation of gI and its incorporation into viral particles. In contrast, deletion of the first cysteine-rich region did not affect viral entry into human tonsil T cells in vitro or into melanoma cells infected with cell-free VZV. These experiments demonstrate that gE/gI heterodimer formation is essential for efficient cell-cell spread and incorporation of gI into viral particles but that it is dispensable for infectious varicella-zoster virion formation and entry into target cells. Blocking gE binding to gI resulted in severe impairment of VZV infection of human skin xenografts in SCIDhu mice in vivo, documenting the importance of cell fusion mediated by this complex for VZV virulence in skin.
Indexed as
Identifiers
What OpenQuestion holds
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.