EBNA2 is required for protection of latently epstein-barr virus-infected B cells against specific apoptotic stimuli

Myun Lee Jae, Kyoung Ho Lee, Christopher J. Farrell, Paul D. Ling, Bettina Kempkes, Han Park Jeon, S. Diane Hayward

Research output: Contribution to journalArticlepeer-review

Abstract

In addition to functioning as a transcriptional transactivator, Epstein-Barr virus EBNA2 interacts with Nur77 to protect against Nur77-mediated apoptosis. Estrogen-regulated EBNA2 in EREB2-5 cells was replaced by either EBNA2 or EBNA2 with a deletion of conserved region 4 (EBNA2ΔCR4). Both EBNA2-converted and EBNA2ΔCR4-converted EREB2-5 cells grew in the absence of estrogen and expressed LMP1. Treatment with tumor necrosis factor alpha did not induce apoptosis of EBNA2- or EBNA2ΔCR4-expressing cells, but EBNA2ΔCR4 cells were susceptible to etoposide and 5-fluorouracil, Nur77-mediaied inducers of apoptosis. Thus, EBNA2 protects B cells against specific apoptotic agents against which LMP1 is not effective.

Original languageEnglish (US)
Pages (from-to)12694-12697
Number of pages4
JournalJournal of virology
Volume78
Issue number22
DOIs
StatePublished - Nov 2004

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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