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EBV Persistence in Memory B Cells In Vivo

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TLDR
It is proposed that EBV indiscriminately infects B cells in mucosal lymphoid tissue and that these cells differentiate to become resting memory B cells that then enter the circulation and persist by exploiting the mechanisms that produce and maintain long-term B cell memory.
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This article is published in Immunity.The article was published on 1998-09-01 and is currently open access. It has received 806 citations till now. The article focuses on the topics: Naive B cell & B-1 cell.

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Epstein–Barr virus: 40 years on

TL;DR: The link between EBV and 'endemic' Burkitt's lymphoma proved consistent and became the first of an unexpectedly wide range of associations discovered between this virus and tumours.
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Epstein-Barr Virus Infection

TL;DR: The Epstein–Barr virus (EBV) was discovered 36 years ago by electron microscopy of cells cultured from Burkitt's lymphoma tissue by Epstein, Achong, and Barr and has been found in tissues from other cancers, including T-cell lymphomas and Hodgkin's disease.
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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.
References
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Journal ArticleDOI

A novel form of Epstein-Barr virus latency in normal B cells in vivo.

TL;DR: It is concluded that the EBV-infected cells in vivo are B cells with a nonactivated phenotype, which represents a novel form of latency in normal B cells.
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In Vivo Ablation of Surface Immunoglobulin on Mature B Cells by Inducible Gene Targeting Results in Rapid Cell Death

TL;DR: A transgenic mouse is generated in which the BCR can be inducibly ablated through V region gene deletion and leads to rapid death of mature B lymphocytes, which is preceded by down- regulation of MHC antigens and up-regulation of CD95 (Fas) and can be delayed by constitutive bcl-2 expression.
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Epstein-Barr Virus LMP2A Drives B Cell Development and Survival in the Absence of Normal B Cell Receptor Signals

TL;DR: LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2a possesses a constitutive signaling activity in nontransformed cells.
Trending Questions (2)
Do memory B cells ever go away?

Thus, EBV may persist by exploiting the mechanisms that produce and maintain long-term B cell memory.

Do B cells work against viruses?

We propose that EBV indiscriminately infects B cells in mucosal lymphoid tissue and that these cells differentiate to become resting memory B cells that then enter the circulation.