Abstract
Epstein-Barr virus (EBV) not only induces growth transformation in human B lymphocytes, but has more recently been shown to enhance B cell survival under suboptimal conditions where growth is inhibited; both effects are mediated through the coordinate action of eight virus-coded latent proteins. The effect upon cell survival is best recognized in EBV-positive Burkitt's lymphoma cell lines where activation of full virus latent gene expression protects the cells from programmed cell death (apoptosis). Here we show by DNA transfection into human B cells that protection from apoptosis is conferred through expression of a single EBV latent protein, the latent membrane protein LMP 1. Furthermore, we demonstrate that LMP 1 mediates this effect by. up-regulating expression of the cellular oncogene bcl-2. The interplay between EBV infection and expression of this cellular oncogene has important implications for virus persistence and for the pathogenesis of virus-associated malignant disease.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1107-1115 |
| Number of pages | 9 |
| Journal | Cell |
| Volume | 65 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jun 28 1991 |
Funding
This work was supported by the Cancer Research Campaign, London, England. M. R. is a Wellcome Senior Research Fellow in Basic Biomedical Sciences. We gratefully acknowledge the gift of the bcl-2/100 and bcl-2/124 monoclonal antibodies made available to us in advance of their publication by Dr. D. Mason, John Radcliffe Hospital, Oxford; Dr. Mason’s laboratory is supported by the Leukaemia Research Fund. We also thank Dr. Y. Tsujimoto for providing the pCAJSV2 and pCAJ bcl-2 plasmids, Dr. R. Longnecker for providing the LMP P-transfected BJAB cell clones, Susan Williams for photographic assistance, and Deborah Williams for typing the manuscript.
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology
