Abstract
The Epstein—Barr virus (EBV) is a widely-spread human herpes virus, that persists latently for the life time of the infected host. The life-long exposure to EBV and the fact that EBV-infected B lymphocytes from the peripheral blood have the potential to proliferate continuously (immortalization), are believed to be predisposing factors for the emergence of EBV-associated human malignancies like Burkitt’s Lymphoma (BL), Nasopharyngeal Carcinoma (NPC), Hodgkin’s disease (HD), and B and T cell lymphomas in immunocompromised individuals [1]. Little is known about the EBV persistence in vivo, and the only models for EBV latency and reactivation are B-cells immortalised in vitro or Burkitt lymphomas cell lines. In such cells, only a minority of the viral genes are expressed and define latency. In this chapter, the molecular mechanisms of EBV-mediated immortalisation of B cells, latency and reactivation will be shortly presented.
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Sergeant, A. (1996). The Epstein-Barr virus latency and reactivation. In: Touraine, J.L., Traeger, J., Bétuel, H., Dubernard, J.M., Revillard, J.P., Dupuy, C. (eds) Cancer in Transplantation: Prevention and Treatment. Transplantation and Clinical Immunology, vol 27. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0175-9_21
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DOI: https://doi.org/10.1007/978-94-009-0175-9_21
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