HODGKINS-DISEASE AND EPSTEIN-BARR-VIRUS

Genome detection: Detection of Epstein-Barr virus (EBV) genome and gen e products in about 40% to 60% of cases of classical Hodgkin's disease (HD) has been made possible by in situ hybridisation methods (EBER RN A) and the production of monoclonal antibodies directed to LMP1 protei ns. The EBV detection rate depends on the histological subtype with th e highest detection rate in mixed cellularity cases (60%) and a comple te lack of detection in cases of lymphocyte predominance HD. Recent ev idence: Several lines of evidence, such as the demonstration of EBV cl onality and the expression of a number of gene products, suggest that in HD EBV is not a simple passenger. Reed-Stemberg cells showed a late nt infection comparable to that found in nasopharyngeal carcinoma (lat ency of type 2: EBNA1+, EBNA2-, LMP1+, EBER RNA+). In HD, EBV replicat ion is observed in only a few cases. Clinic: There ate no clear differ ences between EBV-positive and EBV-negative HD regarding clinical data (stage, response to treatment, disease-free survival and overall surv ival). In addition, the biological parameters (including EBV serology) between the two groups of HD are not different However, EBV-positive HD are more frequent in males with a sex-ratio of 2:1. Perspectives: C urrent investigations are focused on the polymorphism of the EBV genom e with a cluster of point mutations and deletions within the carboxyte rminal region of the LMP1 gene. These mutations may alter the oncogeni c properties of the protein and may be found in cases with aggressive behavior. Recent studies suggest the existence of abnormal local (intr a tumoral) and general cytotoxic responses in patients effected with E BV-positive Hodgkin's disease.