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Journal ArticleDOI

Epstein-Barr virus: exploiting the immune system

David A. Thorley-Lawson
- 01 Oct 2001 - 
- Vol. 1, Iss: 1, pp 75-82
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TLDR
Two genes encoded by the virus — LMP1 and LMP2A — allow EBV to exploit the normal pathways of B-cell differentiation so that the EBV-infected B blast can become a resting memory cell.
Abstract
In vitro, Epstein-Barr virus (EBV) will infect any resting B cell, driving it out of the resting state to become an activated proliferating lymphoblast. Paradoxically, EBV persists in vivo in a quiescent state in resting memory B cells that circulate in the peripheral blood. How does the virus get there, and with such specificity for the memory compartment? An explanation comes from the idea that two genes encoded by the virus--LMP1 and LMP2A--allow EBV to exploit the normal pathways of B-cell differentiation so that the EBV-infected B blast can become a resting memory cell.

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Citations
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Functional delivery of viral miRNAs via exosomes

TL;DR: These findings are consistent with miRNA-mediated gene silencing as a potential mechanism of intercellular communication between cells of the immune system that may be exploited by the persistent human γ-herpesvirus EBV.
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Persistence of the Epstein–Barr Virus and the Origins of Associated Lymphomas

TL;DR: This review of the life cycle of the Epstein–Barr virus explains how EBV establishes lifelong infection in a host with protective immunity against the virus.
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Cellular responses to viral infection in humans: lessons from Epstein-Barr virus.

TL;DR: This experiment of nature provides a system to advance understanding of immunological homeostasis in humans, illustrating how data obtained from the study of EBV have wider significance to the immunological community.
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Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis

TL;DR: It is determined that Epstein-Barr virus infection greatly increased the risk of subsequent multiple sclerosis and that it preceded the development of disease, supporting its potential role in the pathogenesis of multiple sclerosis.
References
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Journal ArticleDOI

Stable replication of plasmids derived from Epstein-Barr virus in various mammalian cells

TL;DR: It is shown that circular DNAs containing oriP, the EBNA-1 gene and a selectable marker replicate autonomously in cells derived from at at least four developmental lineages and from at least three species.
Journal ArticleDOI

The CD40 Antigen and its Ligand

TL;DR: As other members of the tumor necrosis factor receptor family have been shown to bind several ligands, it is possible that CD40 may bind other ligands that may trigger CD40 on different cell types such as hematopoietic cells or epithelial cells.
Journal ArticleDOI

A chemokine-driven positive feedback loop organizes lymphoid follicles

TL;DR: It is established that B-lymphocyte chemoattractant (BLC/BCA1) and its receptor, CXCR5, are needed for B-cell homing to follicles in lymph nodes as well as in spleen, and that BLC is required for the development of most lymph nodes and Peyer's patches.
Journal Article

Notch signaling : Signal transduction

TL;DR: The Notch/Lin-12/Glp-1 receptor family mediates the specification of numerous cell fates during development in Drosophila and Caenorhabditis elegans and putative components of the signaling cascade are identified, including a conserved family of extracellular ligands and two cellular factors that may associate with the Notch Intracellular domain.
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