ArticlePLoS pathogens2014
Assembly and architecture of the EBV B cell entry triggering complex.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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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.
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.
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Who cites it
65 citing papers in PubMed, 94 citations in OpenAlex.
- Transgenic mouse-derived human monoclonal antibodies targeting EBV gp350 and gp42 provide basis for therapeutic development.Cell reports. Medicine · 2026Article
- Pre-assembled complexes and allosteric effects: parallels between eukaryotic phosphorylation cascades and membrane fusion during herpesviral entry.Journal of virology · 2026Review
- Article
- Cyclic-di-GMP interferes with DNA-MucR-DNA bridging to derepress genes targeted by the xenogeneic silencer MucR.Nucleic acids research · 2025Article
- Eph receptor tyrosine kinases are functional entry receptors for murine gammaherpesvirus 68.PLoS pathogens · 2025Article
- A Liposome-Based Nanoparticle Vaccine Induces Effective Immunity Against EBV Infection.Vaccines · 2025Article
- PARP2 Catalytic Activity Is Allosterically Stimulated by Binding to the c-KIT1 G-Quadruplex.ACS omega · 2025Article
- Research landmarks on the 60th anniversary of Epstein-Barr virus.Science China. Life sciences · 2025Review
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- An In Silico Approach to Discover Efficient Natural Inhibitors to Tie Up Epstein-Barr Virus Infection.Pathogens (Basel, Switzerland) · 2024Article
- Genetics of immune response to Epstein-Barr virus: prospects for multiple sclerosis pathogenesis.Brain : a journal of neurology · 2024Article
- 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
- The effect of HLA genotype on disease onset and severity in CTLA-4 insufficiency.Frontiers in immunology · 2024Article
- Neutralizing antibodies against EBV gp42 show potentEmerging microbes & infections · 2023Article
- Non-overlapping epitopes on the gHgL-gp42 complex for the rational design of a triple-antibody cocktail against EBV infection.Cell reports. Medicine · 2023Article
- Mechanisms of T cell evasion by Epstein-Barr virus and implications for tumor survival.Frontiers in immunology · 2023Review
- Urgency and necessity of Epstein-Barr virus prophylactic vaccines.NPJ vaccines · 2022Review
- Review
5 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
11 authors at 4 institutions in 1 country.
Funding
Abstract
Epstein-Barr Virus (EBV) is an enveloped double-stranded DNA virus of the gammaherpesvirinae sub-family that predominantly infects humans through epithelial cells and B cells. Three EBV glycoproteins, gH, gL and gp42, form a complex that targets EBV infection of B cells. Human leukocyte antigen (HLA) class II molecules expressed on B cells serve as the receptor for gp42, triggering membrane fusion and virus entry. The mechanistic role of gHgL in herpesvirus entry has been largely unresolved, but it is thought to regulate the activation of the virally-encoded gB protein, which acts as the primary fusogen. Here we study the assembly and function of the reconstituted B cell entry complex comprised of gHgL, gp42 and HLA class II. The structure from negative-stain electron microscopy provides a detailed snapshot of an intermediate state in EBV entry and highlights the potential for the triggering complex to bring the two membrane bilayers into proximity. Furthermore, gHgL interacts with a previously identified, functionally important hydrophobic pocket on gp42, defining the overall architecture of the complex and playing a critical role in membrane fusion activation. We propose a macroscopic model of the initiating events in EBV B cell fusion centered on the formation of the triggering complex in the context of both viral and host membranes. This model suggests how the triggering complex may bridge the two membrane bilayers, orienting critical regions of the N- and C- terminal ends of gHgL to promote the activation of gB and efficient 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.