Epstein Barr virus can infect B lymphocytes and epithelial cells. Epithelial cells present the natural reservoir for the virus in man. In vitro, infected cells harbor the virus predominantly in a latent state with the expression of a set of nuclear (EBNA 1-6) and latent membrane genes (LMP 1-2) and virus-transformed B cells grow as permanently immortalized lymphoblastoid cell lines, that show increased resistance to various growth inhibiting factors. Here we show that the lymphoma-associated oncogene BCL-2 is upregulated by different latent Epstein-Barr virus genes in B lymphocytes as well as keratinocyte cell lines. Thus, the induction of BCL-2 gene expression seems to be part of the survival strategy of the virus independently of the host cell infected.