Reactivation of Epstein-Barr virus from latency.
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.
Amon
Wolfgang
W
Ludwig Institute for Cancer Research and Department of Virology, Imperial College Faculty of Medicine, St Mary's Campus, Norfolk Place, London W2 1PG, UK.
Farrell
Paul J
PJ
D002051:Burkitt Lymphoma / Q000188:drug therapy / Q000821:virology*; D045744:Cell Line, Tumor; D004268:DNA-Binding Proteins / Q000235:genetics; D020031:Epstein-Barr Virus Infections / Q000821:virology*; D015870:Gene Expression; D016679:Genome, Viral; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000502:physiology*; D006689:Hodgkin Disease / Q000821:virology; D006801:Humans; D009303:Nasopharyngeal Neoplasms / Q000188:drug therapy / Q000821:virology; D015534:Trans-Activators / Q000235:genetics; D014764:Viral Proteins / Q000235:genetics; D014775:Virus Activation; D017735:Virus Latency
C063676:BZLF1 protein, Herpesvirus 4, Human; D004268:DNA-Binding Proteins; D015534:Trans-Activators; D014764:Viral Proteins