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 language | English (US) |
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Pages (from-to) | 12694-12697 |
Number of pages | 4 |
Journal | Journal of virology |
Volume | 78 |
Issue number | 22 |
DOIs | |
State | Published - Nov 2004 |
ASJC Scopus subject areas
- Microbiology
- Immunology
- Insect Science
- Virology