Epstein-Barr virus in Hodgkin's disease: more than just an innocent bystander.

Several lines of evidence suggest that the Epstein-Barr virus (EBV) is an important factor in the pathogenesis of Hodgkin's disease (HD). This Editorial focuses on two pathogenic mechanisms probably influenced by the presence of EBV in the Hodgkin and Reed-Sternberg (H-RS) cells: resistance of the H-RS cells to apoptosis; and escape of H-RS cells from a cytotoxic T lymphocyte (CTL) mediated immune response. In addition, data are summarized implicating the latent membrane protein 1 (LMP1) as the most likely EBV-encoded protein responsible for this putative EBV-mediated pathogenic effect. It is known that, using conventional therapy regimens, the presence of EBV bears little influence on clinical presentation and treatment outcome of HD. However, the differences in regulation of both apoptosis and immune escape mechanisms between EBV+ and EBV- cases may be important determinants of the success of immunotherapy to treat Hodgkin's disease. Thus, clarification of these mechanisms will be essential to the development of successful immunotherapeutic strategies in Hodgkin's disease.