Epstein-Barr Virus (EBV) effectively transforms B lymphocytes into lon
g-term cell lines or tumors through the interaction of viral gene prod
ucts and cellular proteins induced secondary to the virus infection. T
he latent membrane protein (LMP) gene, the EBV nuclear antigens (EBNAs
) 1 and 2, and the origin of replication genes of the virus are the pr
incipal viral effecters of transformation. One of the cellular protein
s that enhances the growth and proliferation of B cells is lymphotoxin
(LT). We have found that Burkitt's lymphoma cells containing a strain
of EBV with a deletion in EBNA-2 had lower constitutive and inducible
levels of LT compared to LT production in Burkitt's cells with compet
ent EBV or lymphoblastoid cell lines actively producing EBV. Also, the
LT production in the latter cell lines was greater than in cells in w
hich the infecting EBV had a deletion in the LMP gene. The relative de
crease in LT production associated with deletions in the LMP was less
than that found with EBNA-2 deletions. Overall our results indicate th
at the EBNA-2 gene enhances the capacity of EBV-infected cells to prod
uce LT. (C) 1997 Academic Press, Inc.