Epstein Barr virus can infect B lymphocytes and epithelial cells. Epit
helial cells present the natural reservoir for the virus in man. In vi
tro, infected cells harbor the virus predominantly in a latent state w
ith 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 immo
rtalized lymphoblastoid cell lines, that show increased resistance to
various growth inhibiting factors. Here we show that the lymphoma-asso
ciated 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 surviv
al strategy of the virus independently of the host cell infected.