Epstein-Barr virus LMP2A imposes sensitivity to apoptosis

Michelle Swanson-Mungerson*, Rebecca Bultema, Richard Longnecker

*Corresponding author for this work

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

In cell lines, the Epstein-Barr virus (EBV)-encoded protein latent membrane protein 2A (LMP2A) protects B-cells from apoptosis by blocking B-cell receptor (BCR) signalling. However, EBV-infected B-cells in vivo are extremely different from cell lines. This study used a murine transgenic model in which B-cells express LMP2A and a BCR specific for hen egg lysozyme to determine whether LMP2A protects resting and antigen-activated B-cells from apoptosis. LMP2A allows BCR signal transduction and induces constitutive activation of NF-κB to increase Bcl-2 levels that afford LMP2A-mediated protection from apoptosis in the absence or presence of antigen. In contrast, low levels of NF-κB inhibitor only affected Bcl-2 and Bcl-xL levels and increased apoptosis in LMP2A-negative B-cells after BCR cross-linking. These data suggest that LMP2A uniquely makes resting B-cells sensitive to NF-κB inhibition and apoptosis and suggest that NF-κB may be a novel target to eradicate latently EBV-infected B-cells.

Original languageEnglish (US)
Pages (from-to)2197-2202
Number of pages6
JournalJournal of General Virology
Volume91
Issue number9
DOIs
StatePublished - Sep 2010

ASJC Scopus subject areas

  • Virology

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