Fol. Biol. 2004, 50, 131-135
Non-proliferative Interactions of Epstein-Barr Virus and Human B Lymphocytes
Epstein-Barr virus (EBV) and man have a long common history, during which both evolved strategies leading to a largely harmless coexistence (Klein, 1994; Rickinson and Kieff, 2001). The virus was detected in 1965, in cultured cells of an African Burkitt lymphoma (BL). Its capacity to transform and immortalize human B lymphocytes in vitro was shown soon thereafter and therefore it was assumed that the lymphoma is induced by EBV (Küppers, 2003). However, the discovery of EBV-negative lymphomas with similar pathology and carrying a for BL common, typical cytogenetic marker indicated that even if the virus can contribute to the development of this malignancy, it is not responsible for proliferation of the tumour cells. The cytogenetical change is a reciprocal chromosomal translocation between chromosome 8 and either chromosome 14, 2 or 22. In such cells the expression of the myc oncogene (chr. 8) is constitutive due to its regulation by the juxtaposed immunoglobulin (heavy, chr 14, or light chains, chr 2 or 22) genes. The active myc gene drives the cells for division. Whether and how EBV can have a role in the aetiology of BL is still not clarified.
Funding
The work was supported by the Swedish Cancer Society and by the Cancer Research Institute (New York)/Concern Foundation (Los Angeles).
References
Copyright
This is an open-access article distributed under the terms of the Creative Commons Attribution License.