Abstract
Epstein-Barr virus (EBV) is a ubiquitous human herpes virus with the unique ability to immortalize primary resting human B lymphocytes. The virus is the causative agent of infectious mononucleosis and is associated with a number of human malignancies including Burkitt’s Lymphoma, Nasopharyngeal Carcinoma, Hodgkin’s Disease, and Immunoblastic Lymphoma arising in immunocompromized individuals (for review, see Rickinson and KiefF, 1995). The pathogenicity of the virus is closely linked to its immortalizing capacity. Studying the role of EBV in B cell immortalization may thus help to better understand the role of the virus in disease pathogenesis. In EBV immortalized cells only a limited set of viral gene products is expressed including six nuclear (EBNA1, EBNA2, EBNA3A, -3B, -3C and EBNA-LP) and two membrane proteins (LMP1 and LMP2) (for review, see Kieff, 1995). For several reasons EBNA2 plays a pivotal role in B cell immortalization: (i) deletion of the EBNA2 gene leads to the loss of the immortalizing capacity of the virus, (ii) EBNA2, together with EBNA-LP, is the first viral gene expressed in infected B cells, and (iii) EBNA2 is a transcriptional regulator acting as a master switch regulating the expression of a number of cellular genes (e.g. CD21 and CD23) and viral genes involved in B cell immortalization. Amongst the viral genes regulated by EBNA2 are the LMP1 and LMP2 genes and the large transcription unit giving rise to EBNA-LP and EBNA2 as well as the family of EBNA3 proteins. EBNA2 exerts its function as a transcriptional regulator without binding to DNA directly. It is thus of primary importance to elucidate the molecular mechanism of action of EBNA2.
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© 1999 Springer-Verlag Berlin Heidelberg
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Zimber-Strobl, U. et al. (1999). EBNA2 and c-myc in B Cell Immortalization by Epstein-Barr Virus and in the Pathogenesis of Burkitt’s Lymphoma. In: Melchers, F., Potter, M. (eds) Mechanisms of B Cell Neoplasia 1998. Current Topics in Microbiology and Immunology, vol 246. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60162-0_39
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DOI: https://doi.org/10.1007/978-3-642-60162-0_39
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