BURKITTS-LYMPHOMA CELLS ARE RESISTANT TO PROGRAMMED CELL-DEATH IN THEPRESENCE OF THE EPSTEIN-BARR-VIRUS LATENT ANTIGEN EBNA-4

Group I Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cell s display a surface phenotype characteristic of germinal centre B cell s and readily undergo apoptosis in response to a variety of stimuli, i ncluding serum deprivation. Activation of EBV latent gene expression h as been shown to increase the survival of these tumour cells by blocki ng programmed cell death. To investigate the nature of this protection , we assessed the function of the EBV latent EBNA-4 gene in a group I lymphoma line, dG75. Group I BL cells induced to undergo apoptosis in response to serum starvation were protected in the presence of EBNA-4 protein. A possible factor underlying this EBNA-4-associated survival was increased expression of the oncoprotein bcl-2, a known repressor o f cell death. Together these data suggest that EBNA-4 plays an importa nt role in the regulation of programmed cell death in BL tumour cells. (C) 1995 Wiley-Liss, Inc.