Viruses and cancer risks: outgrowth of Epstein-Barr virus-positive Burkitt's lymphoma in the immune host.

This work examines ways in which Epstein-Barr (EB) virus-positive Burkitt's lymphoma (BL) cells achieve outgrowth in vivo in the face of prevailing EB virus-specific cytotoxic T-cell surveillance. Earlier work has shown that some, but not all, BL cell lines in vitro are insensitive to virus-specific T-cell cytolysis and the present study identifies two mechanisms whereby the tumour cells might evade detection. First, BL-cell lines which stably retain the original tumour cell phenotype on serial passage in vitro show very low expression of two cell adhesion-related molecules, LFA-1 and ICAM 1, and are negative for a third such molecule, LFA-3; these molecules are thought to play a crucial role in the non antigen-dependent phase of effector: target cell conjugation which precedes antigen-specific recognition and target cell lysis. Secondly, those same BL cell lines display an unusually restricted pattern of EB virus latent gene expression with at least two potentially important target proteins for the T-cell response, namely EBNA 2 and LMP, not detectably expressed.