EBV is associated to the development of several malignancies of lymphoid and epithelial origin, including Burkitts Lymphoma, post-transplant lymphoproliferative disorders, Hodgkins disease, AIDS-associated lymphomas, NK/T cell lymphoma and Nasopharyngeal carcinoma. EBV genes play an essential role in the development of the malignant phenotype and therefore molecules interfering with the function of these genes may represent an essential tool to treat EBV-associated malignancies. Several strategies to inhibit virus-induced tumorigenesis have been developed including antiviral and antitumor molecules, gene therapy approaches, interference with epigenetic regulatory mechanisms, adoptive and active immunotherapeutic protocols. While gene therapy and epigenetic approaches gave inconsistent results, immunological therapies using ex vivo expanded autologous and allogenic cells specific for EBV have obtained promising results. The major challenge is now to improve the current knowledge on virus replication strategies and on the characteristics of protective immune response that may result in more effective therapeutic protocols.
Keywords: EBV, Burkitt's Lymphoma, Hodgkin's disease, AIDS-associated lymphomas, NK/T cell lymphoma, Nasopharyngeal carcinoma, tumorigenesis, antitumor molecules, allogenic cells, EPSTEIN BARR VIRUS
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