ArticlePLoS pathogens2011
Epstein-Barr virus infection of polarized epithelial cells via the basolateral surface by memory B cell-mediated transfer infection.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Antibodies Against Epstein-Barr Virus as Disease Markers of Gastric Cancer: A Systematic Review.Technology in cancer research & treatmentPooled it
- Epstein-Barr Virus and Multiple Sclerosis: Mechanistic Insights into Virus-Driven Autoimmunity.Microorganisms · 2026Review
- Immune hub genes and a proof-of-concept prognostic signature in EBV-associated gastric carcinoma.iScience · 2026Article
- Uncovering genetic variation in humoral inborn errors of immunity in African populations: insights from the African genome variation database.Scientific reports · 2026Article
- Progress and prospects for herpesvirus vaccination using gB antigens.Frontiers in immunology · 2026Review
- Relationship between Epstein-Barr virus and inflammatory bowel disease.World journal of gastroenterology · 2025Review
- Gastrointestinal inflammation and cancer: viral and bacterial interplay.Gut microbes · 2025Review
- Epstein-Barr Virus in Multiple Sclerosis: Past, Present, and Future.Neurology(R) neuroimmunology & neuroinflammation · 2025Review
- Epstein-Barr virus pathogenesis and emerging control strategies.Nature reviews. Microbiology · 2025Review
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- Heat shock factor 2 regulates oncogenic gamma-herpesvirus gene expression by remodeling the chromatin at the ORF50 and BZLF1 promoter.PLoS pathogens · 2025Article
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- The landscape of 142 Epstein-Barr viral whole genomes in gastric cancer.Journal of gastroenterology · 2025Article
- Tissue and cellular tropism ofVeterinary pathology · 2024Article
- Characterization of latently infected EBV+ antibody-secreting B cells isolated from ovarian tumors and malignant ascites.Frontiers in immunology · 2024Article
- Detection of Epstein-Barr virus infection in primary junctional epithelial cell cultures.Journal of oral microbiology · 2024Article
- Cytokine Storm Syndromes Associated with Epstein-Barr Virus.Advances in experimental medicine and biology · 2024Review
- Epstein‑Barr virus as a promoter of tumorigenesis in the tumor microenvironment of breast cancer (Review).International journal of molecular medicine · 2023Review
- Updates on Epstein-Barr Virus (EBV)-Associated Nasopharyngeal Carcinoma: Emphasis on the Latent Gene Products of EBV.Medicina (Kaunas, Lithuania) · 2022Review
- Cell-in-Cell: From Cell Biology to Translational Medicine.BioMed research international · 2022Review
15 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Epstein Barr virus (EBV) exhibits a distinct tropism for both B cells and epithelial cells. The virus persists as a latent infection of memory B cells in healthy individuals, but a role for infection of normal epithelial is also likely. Infection of B cells is initiated by the interaction of the major EBV glycoprotein gp350 with CD21 on the B cell surface. Fusion is triggered by the interaction of the EBV glycoprotein, gp42 with HLA class II, and is thereafter mediated by the core fusion complex, gH/gL/gp42. In contrast, direct infection of CD21-negative epithelial cells is inefficient, but efficient infection can be achieved by a process called transfer infection. In this study, we characterise the molecular interactions involved in the three stages of transfer infection of epithelial cells: (i) CD21-mediated co-capping of EBV and integrins on B cells, and activation of the adhesion molecules, (ii) conjugate formation between EBV-loaded B cells and epithelial cells via the capped adhesion molecules, and (iii) interaction of EBV glycoproteins with epithelial cells, with subsequent fusion and uptake of virions. Infection of epithelial cells required the EBV gH and gL glycoproteins, but not gp42. Using an in vitro model of normal polarized epithelia, we demonstrated that polarization of the EBV receptor(s) and adhesion molecules restricted transfer infection to the basolateral surface. Furthermore, the adhesions between EBV-loaded B cells and the basolateral surface of epithelial cells included CD11b on the B cell interacting with heparan sulphate moieties of CD44v3 and LEEP-CAM on epithelial cells. Consequently, transfer infection was efficiently mediated via CD11b-positive memory B cells but not by CD11b-negative naïve B cells. Together, these findings have important implications for understanding the mechanisms of EBV infection of normal and pre-malignant epithelial cells in vivo.
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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.