Epstein-Barr virus mediates a switch in responsiveness to transforming growth factor, type beta, in cells of the B cell lineage.

The functional performance of the transforming growth factor beta (TGF beta), appears to depend on the target cell phenotype as well as in vitro culture conditions. We show here that Epstein-Barr virus (EBV)-infection may induce a change in responsiveness to TGF beta, since TGF beta inhibits traverse of the cell cycle of activated normal human B cells, but promotes cell proliferation of EBV-positive Burkitt's lymphoma cell lines as well as EBV-infected B cells. We present evidence that the switch in the responsiveness to TGF beta is mediated by EBV infection, irrespective of the proliferative status of target cells, and thus may contribute to the initiation as well as the maintenance of certain B cell neoplasias.