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Studies on the Prevention of EBV-induced Malignancies by a Sub-unit Antiviral Vaccine

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Vaccine Intervention Against Virus-Induced Tumours
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Abstract

Epstein-Barr virus (EBV) was discovered 20 years ago1. Since that time an immense body of information has been accumulated on all aspects of the agent, and much of its general biology, molecular biology and behaviour in populations has become clear2, 3. In the course of this work, efforts from many laboratories have established remarkably close associations between EBV and certain particular human cancers — namely, endemic Burkitt’s lymphoma (BL)4, 5, the undifferentiated form of nasopharyngeal carcinoma (NPC)6 and the lymphomas which occur in immunosuppressed allograft patients with an unusually high frequency7–9. The basis of these associations is well known10–12, and recent studies on cellular oncogene activation suggest possible explanations, at least in the case of endemic BL. Thus, in endemic BL, EBV appears to play its role by infecting, and thereby ‘immortalising’, a pool of B lymphocytes whose virus-driven continuous cell divisions facilitate any one of three characteristic chromosomal translocations each of which can activate the c-myc oncogene13. However, since EBV is widespread in all human populations, whereas the areas where BL has a high incidence are remarkably restricted, it has long been recognised that there must be yet another element in the equation, functioning as a cofactor along with the virus and determining the geographical distribution of the endemic tumour. Suggestive epidemiological evidence has in the past been used to support the notion that hyperendemic malaria was the likely cofactor14.

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© 1986 The Leukaemia Research Fund

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Epstein, M.A. (1986). Studies on the Prevention of EBV-induced Malignancies by a Sub-unit Antiviral Vaccine. In: Goldman, J.M., Epstein, M.A. (eds) Vaccine Intervention Against Virus-Induced Tumours. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-08243-8_3

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  • DOI: https://doi.org/10.1007/978-1-349-08243-8_3

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