EPSTEIN-BARR-VIRUS AND ITS INTERACTION WITH THE HOST

Epstein-Barr virus (EBV) as a member of the herpesvirus family persist s lifelong in the human body and causes diseases associated with virus replication (infectious mononucleosis, oral hairy leukoplakia) as wel l as neoplastic conditions such as nasopharyngeal carcinoma, B-cell ly mphoma, Hodgkin's disease associated with viral latency. This complex biology relates to a highly regulated control of the persisting virus. Still, EBV is lytically produced in certain compartments of the human body. Epithelial cells were found to be of key importance for this. V arious routes (cell fusion, IgA receptor-mediated uptake) were describ ed for EBV to enter epithelial cells in the absence of CR2 receptor. V iral entry into cells, however, via CR2 receptor fusion or IgA mediate d was not found to be sufficient for viral production. The molecular m echanisms for the lack of viral production in most target cells are pr imarily the presence of silencer activities and the early elimination of cells entering the lytic cycle. Only terminally differentiated epit helial cells are capable of supporting an efficient lytic cycle of EBV replication. EBV-mediated suppression of apoptosis as well as down-re gulation of cellular and viral gene products, such as HLA molecules, w hich mediate recognition by the immune system, are important contribut ing factors to the development of these neoplasias where viral genes, possibly via interaction with anti-oncogenes, such as p53, in context with genetic and environmental factors play a key role. Novel diagnost ic tools and a vaccine have been developed which could help to control EBV-related diseases.