ArticleJournal of virology2017
Epstein-Barr Virus Fusion with Epithelial Cells Triggered by gB Is Restricted by a gL Glycosylation Site.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Proteomics Combined with N-Glycoproteomics to Explore the Pathogenesis of Nasopharyngeal Carcinoma.Journal of proteome research · 2025Article
- Desmocollin 2 is a dominant entry receptor for Epstein-Barr virus infection of epithelial cells.Nature microbiology · 2025Article
- Epstein-Barr virus exploits desmocollin 2 as the principal epithelial cell entry receptor.Nature microbiology · 2025Article
- HPV6-Induced Gene Expression Signature in Recurrent Respiratory Papillomatosis.The Laryngoscope · 2025Article
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- Advances in cellular and molecular pathways of salivary gland damage in Sjögren's syndrome.Frontiers in immunology · 2024Review
- Neutralizing antibodies against EBV gp42 show potentEmerging microbes & infections · 2023Article
- Functional diversity: update of the posttranslational modification of Epstein-Barr virus coding proteins.Cellular and molecular life sciences : CMLS · 2022Review
- A Neutralizing Antibody Targeting gH Provides Potent Protection against EBV ChallengeJournal of virology · 2022Article
- Glycoprotein B Antibodies Completely Neutralize EBV Infection of B Cells.Frontiers in immunology · 2022Article
- Review
- Epstein-Barr Virus-Encoded Latent Membrane Protein 2A Downregulates GCNT3 via the TGF-β1/Smad-mTORC1 Signaling Axis.Journal of virology · 2021Article
- Main Targets of Interest for the Development of a Prophylactic or Therapeutic Epstein-Barr Virus Vaccine.Frontiers in microbiology · 2021Review
- Epstein-Barr Virus gH/gL and Kaposi's Sarcoma-Associated Herpesvirus gH/gL Bind to Different Sites on EphA2 To Trigger Fusion.Journal of virology · 2020Article
- HLA-DPB1 and Epstein-Barr virus gp42 protein jointly contribute to the development of Hodgkin lymphoma.Translational cancer research · 2020Article
- Epstein-Barr Virus and Systemic Autoimmune Diseases.Frontiers in immunology · 2020Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) entry into epithelial cells is mediated by the conserved core fusion machinery, composed of the fusogen gB and the receptor-binding complex gH/gL. The heterodimeric gH/gL complex binds to the EBV epithelial cell receptor or gp42, which binds to the B-cell receptor, triggering gB-mediated fusion of the virion envelope with cellular membranes. Our previous study found that the gL glycosylation mutant N69L/S71V had an epithelial cell-specific hyperfusogenic phenotype. To study the influence of this gL mutant on the initiation and kinetics of gB-driven epithelial cell fusion, we established a virus-free split-green fluorescent protein cell-cell fusion assay that enables real-time measurements of membrane fusion using live cells. The gL_N69L/S71V mutant had a large increase in epithelial cell fusion activity of up to 300% greater than that of wild-type gL starting at early time points. The hyperfusogenicity of the gL mutant was not a result of alterations in complex formation with gH or alterations in cellular localization. Moreover, the hyperfusogenic phenotype of the gL mutant correlated with the formation of enlarged syncytia. In summary, our present findings highlight an important role of gL in the kinetics of gB-mediated epithelial cell fusion, adding to previous findings indicating a direct interaction between gL and gB in EBV membrane fusion.
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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.