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Oncogene. 2003 Aug 11;22(33):5108-21.

Epstein-Barr virus and oncogenesis: from latent genes to tumours.

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  • 1Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. L.S.Young@bham.ac.uk

Abstract

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with the development of both lymphoid and epithelial tumours. As a common virus infection, EBV appears to have evolved to exploit the process of B cell development to persist as a life-long asymptomatic infection. However, the virus can contribute to oncogenesis as evidenced by its frequent detection in certain tumours, namely Burkitt's lymphoma (BL), post-transplant B cell lymphomas, Hodgkin's disease (HD) and nasopharyngeal carcinoma (NPC), and by its unique ability to efficiently transform resting B cells in vitro into permanently growing lymphoblastoid cell lines (LCLs). These transforming effects are associated with the restricted expression of EBV genes such that only a subset of so-called latent virus proteins are expressed in virus infected tumours and in LCLs. Distinct forms of EBV latency are manifest in the different tumours and these appear to be a vestige of the pattern of latent gene expression used by the virus during the establishment of persistent infection within the B cell pool. This review summarises our current knowledge of EBV latent gene function and how this relates to the role of the virus in the aetiology of different tumours.

PMID:
12910248
[PubMed - indexed for MEDLINE]
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