Journal
SEMINARS IN CANCER BIOLOGY
Volume 11, Issue 6, Pages 415-421Publisher
ACADEMIC PRESS LTD
DOI: 10.1006/scbi.2001.0408
Keywords
Epstein-Barr virus; lymphoma; phosphatidylinositol 3-kinase; PKB; STAT
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Epstein-Barr virus (EBV) uses many different strategies to induce lymphocyte proliferation and survival. In the different states of EBV infection and latency, several genes play specific roles in the induction of cell growth and cell survival proteins. EBNA2A, EBNA-LP and EBNA3C all modulate early events in the G1 phase of the cell cycle. Furthermore, interleukin-6 and interleukin-10, which are induced following EBV infection, appear to be important for growth. They activate signalling pathways that have been shown to link directly to proliferation. Latent membrane protein I (LMP1) induces a number of anti-apoptotic proteins via NF-kappaB, and LMP2A also appears to contribute to lymphocyte survival. This paper describes some of the many cellular pathways modulated by EBV that interact with the signalling machinery and th us make lymphocytes survive and grow.
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