Reactivation of Epstein-Barr virus from latency
Version of Record online: 16 NOV 2004
Copyright © 2004 John Wiley & Sons, Ltd.
Reviews in Medical Virology
Volume 15, Issue 3, pages 149–156, May/June 2005
How to Cite
Amon, W. and Farrell, P. J. (2005), Reactivation of Epstein-Barr virus from latency. Rev. Med. Virol., 15: 149–156. doi: 10.1002/rmv.456
- Issue online: 25 APR 2005
- Version of Record online: 16 NOV 2004
- Manuscript Accepted: 13 SEP 2004
The general problem in cancer treatment centres on finding agents that specifically affect cancer cells without damaging normal cells. The differences between cancer cells and normal cells are usually very subtle but about 15% of all human cancers involve a virus infection, for example the Epstein-Barr virus associated cancers. In these cancers, every tumour cell carries the virus in a latent infection but the number of normal cells infected is very low. So a treatment that could somehow cause the elimination of EBV infected cells would be very specific for the cancer in such cases. One potential approach could involve finding ways to reactivate the latent virus in cancer cells into the early part of the lytic cycle, impeding cell proliferation, targeting chemotherapeutic agents to the cancer and causing the cancer cells to become targets for immune surveillance. This review considers the mechanisms by which EBV reactivation is controlled and discusses possible therapeutic approaches. Copyright © 2004 John Wiley & Sons, Ltd.