| Epstein-Barr Virus Infection of Polarized Epithelial Cells via the Basolateral Surface by Memory B Cell-Mediated Transfer Infection. | |
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MedLine Citation:
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PMID: 21573183 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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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Authors:
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Claire Shannon-Lowe; Martin Rowe |
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Publication Detail:
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Type: Journal Article Date: 2011-05-05 |
Journal Detail:
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Title: PLoS pathogens Volume: 7 ISSN: 1553-7374 ISO Abbreviation: PLoS Pathog. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101238921 Medline TA: PLoS Pathog Country: United States |
Other Details:
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Languages: eng Pagination: e1001338 Citation Subset: IM |
Affiliation:
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Cancer Research UK Birmingham Cancer Centre, School of Cancer Sciences, College of Medical and Dental Sciences, The University of Birmingham, Birmingham, United Kingdom. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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