Epstein-Barr virus (EBV) LMP2A alters normal transcriptional regulation following B-cell receptor activation

Toni Portis, Richard Longnecker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

The latent membrane protein 2A (LMP2A) of Epstein-Barr virus (EBV) is an important mediator of viral latency in infected B-lymphocytes. LMP2A inhibits B-cell receptor (BCR) signaling in vitro and allows for the survival of BCR-negative B cells in vivo. In this study, we compared gene transcription in BCR-activated B cells from non-transgenic and LMP2A Tg6 transgenic mice. We found that the transcriptional induction and down-regulation of many genes that normally occurs in B cells following BCR activation did not occur in B cells from LMP2A Tg6 transgenic mice. Furthermore, LMP2A induced the expression of various transcription factors and genes associated with DNA/RNA metabolism, which may allow for the altered transcriptional regulation observed in BCR-activated B cells from LMP2A Tg6 mice. These results suggest that LMP2A may inhibit the downstream effects of BCR signaling by directly or indirectly altering gene transcription to ensure EBV persistence in infected B cells.

Original languageEnglish (US)
Pages (from-to)524-533
Number of pages10
JournalVirology
Volume318
Issue number2
DOIs
StatePublished - Jan 20 2004

Keywords

  • B cells
  • B-cell receptor
  • Epstein-Barr virus
  • LMP2A
  • Latency
  • Microarray

ASJC Scopus subject areas

  • Virology

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