ReviewMolecules and cells2016
Structural and Mechanistic Insights into the Tropism of Epstein-Barr Virus.
Review in Molecules and cells, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 62 citations in OpenAlex.
- Epstein-Barr Virus-Mediated Apoptosis Evasion in Epithelial Malignancies: Molecular Mechanisms and Therapeutic Implications.Biology · 2026Review
- Epstein-Barr virus receptors: classification, functional mechanisms, and pathogenic implications.Journal of virology · 2026Review
- A potent human neutralizing antibody targeting the receptor-binding site in the glycoprotein gp350 of Epstein-Barr virus.Science China. Life sciences · 2026Article
- Study on the Modes of Cell Death in Lung Cancer Epithelial Cells During Acute EBV Infection Using a Co-Culture Model.Thoracic cancer · 2026Article
- Elevated levels of advanced glycation end-products AGE10 in patients with reactive arthritis caused by Chlamydia trachomatis and Epstein-Barr virus infection.Immunologic research · 2026Article
- Mechanisms of Epstein-Barr virus-associated autoimmunity: a comparative overview.Frontiers in immunology · 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
- Identified receptors shed light on Epstein-Barr virus infection.Nature microbiology · 2025Article
- An insect cell-derived extracellular vesicle-based gB vaccine elicits robust adaptive immune responses against Epstein-Barr virus.Science China. Life sciences · 2025Article
- 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
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- GB and gH/gL fusion machinery: a promising target for vaccines to prevent Epstein-Barr virus infection.Archives of virology · 2024Review
- A cocktail nanovaccine targeting key entry glycoproteins elicits high neutralizing antibody levels against EBV infection.Nature communications · 2024Article
- Neutralizing antibodies against EBV gp42 show potentEmerging microbes & infections · 2023Article
- Wildebeest-Derived Malignant Catarrhal Fever: A Bovine Peripheral T Cell Lymphoma Caused by Cross-Species Transmission ofViruses · 2023Review
- Urgency and necessity of Epstein-Barr virus prophylactic vaccines.NPJ vaccines · 2022Review
- Review
- Immunization with a self-assembling nanoparticle vaccine displaying EBV gH/gL protects humanized mice against lethal viral challenge.Cell reports. Medicine · 2022Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is the prototypical γ-herpesvirus and an obligate human pathogen that infects mainly epithelial cells and B cells, which can result in malignancies. EBV infects these target cells by fusing with the viral and cellular lipid bilayer membranes using multiple viral factors and host receptor(s) thus exhibiting a unique complexity in its entry machinery. To enter epithelial cells, EBV requires minimally the conserved core fusion machinery comprised of the glycoproteins gH/gL acting as the receptor-binding complex and gB as the fusogen. EBV can enter B cells using gp42, which binds tightly to gH/gL and interacts with host HLA class II, activating fusion. Previously, we published the individual crystal structures of EBV entry factors, such as gH/gL and gp42, the EBV/host receptor complex, gp42/HLA-DR1, and the fusion protein EBV gB in a postfusion conformation, which allowed us to identify structural determinants and regions critical for receptor-binding and membrane fusion. Recently, we reported different low resolution models of the EBV B cell entry triggering complex (gHgL/gp42/HLA class II) in "open" and "closed" states based on negative-stain single particle electron microscopy, which provide further mechanistic insights. This review summarizes the current knowledge of these key players in EBV entry and how their structures impact receptor-binding and the triggering of gB-mediated fusion.
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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.