ArticleNature communications2016
Structural basis for Epstein-Barr virus host cell tropism mediated by gp42 and gHgL entry glycoproteins.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed.
- Mechanisms and therapeutic implications of galectins regulating Epstein-Barr virus infection.Virus research · 2026Review
- Transgenic mouse-derived human monoclonal antibodies targeting EBV gp350 and gp42 provide basis for therapeutic development.Cell reports. Medicine · 2026Article
- Enhanced rhLCV production in lymphoblastoid cell lines derived from rhLCV-infected cynomolgus macaque PBMCs.Journal of virology · 2026Article
- Pre-assembled complexes and allosteric effects: parallels between eukaryotic phosphorylation cascades and membrane fusion during herpesviral entry.Journal of virology · 2026Review
- A multi-glycoprotein synergized recombinant virus system resolved the research dilemma of Epstein-Barr virus entry and facilitated the development of entry-specific drugs or vaccines.Current research in microbial sciences · 2026Article
- Desmocollin 2 is a dominant entry receptor for Epstein-Barr virus infection of epithelial cells.Nature microbiology · 2025Article
- A Comparative Genomic Analysis of Epstein-Barr Virus Strains with a Focus on EBV2 Variability.International journal of molecular sciences · 2025Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Research landmarks on the 60th anniversary of Epstein-Barr virus.Science China. Life sciences · 2025Review
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
- Acute intracranial EBV and CMV infections after chemoimmunotherapy for EBV-associated nasopharyngeal carcinoma: a case report and literature review.Frontiers in oncology · 2025Article
- The hidden impact of producer cells on virion composition and infectivity.Future virology · 2025Article
- Targeting RSV-neutralizing B cell receptors with anti-idiotypic antibodies.Cell reports · 2024Article
- GB and gH/gL fusion machinery: a promising target for vaccines to prevent Epstein-Barr virus infection.Archives of virology · 2024Review
- A gH/gL-encoding replicon vaccine elicits neutralizing antibodies that protect humanized mice against EBV challenge.NPJ vaccines · 2024Article
- Potent human monoclonal antibodies targeting Epstein-Barr virus gp42 reveal vulnerable sites for virus infection.Cell reports. Medicine · 2024Article
- Epstein-Barr virus gp42 antibodies reveal sites of vulnerability for receptor binding and fusion to B cells.Immunity · 2024Article
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Neutralizing antibodies against EBV gp42 show potentEmerging microbes & infections · 2023Article
17 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
Herpesvirus entry into host cells is mediated by multiple virally encoded receptor binding and membrane fusion glycoproteins. Despite their importance in host cell tropism and associated disease pathology, the underlying and essential interactions between these viral glycoproteins remain poorly understood. For Epstein-Barr virus (EBV), gHgL/gp42 complexes bind HLA class II to activate membrane fusion with B cells, but gp42 inhibits fusion and entry into epithelial cells. To clarify the mechanism by which gp42 controls the cell specificity of EBV infection, here we determined the structure of gHgL/gp42 complex bound to an anti-gHgL antibody (E1D1). The critical regulator of EBV tropism is the gp42 N-terminal domain, which tethers the HLA-binding domain to gHgL by wrapping around the exterior of three gH domains. Both the gp42 N-terminal domain and E1D1 selectively inhibit epithelial-cell fusion; however, they engage distinct surfaces of gHgL. These observations clarify key determinants of EBV host cell tropism.
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