EBV and Apoptosis: The Viral Master Regulator of Cell Fate?

Research output: Contribution to journalReview article

Authors

Colleges, School and Institutes

External organisations

  • Molecular Genetics of Cancer Division, The Walter and Eliza Hall Institute for Medical Research
  • Department of Medical Biology, The University of Melbourne

Abstract

Epstein-Barr virus (EBV) was first discovered in cells from a patient with Burkitt lymphoma (BL), and is now known to be a contributory factor in 1-2% of all cancers, for which there are as yet, no EBV-targeted therapies available. Like other herpesviruses, EBV adopts a persistent latent infection in vivo and only rarely reactivates into replicative lytic cycle. Although latency is associated with restricted patterns of gene expression, genes are never expressed in isolation; always in groups. Here, we discuss (1) the ways in which the latent genes of EBV are known to modulate cell death, (2) how these mechanisms relate to growth transformation and lymphomagenesis, and (3) how EBV genes cooperate to coordinately regulate key cell death pathways in BL and lymphoblastoid cell lines (LCLs). Since manipulation of the cell death machinery is critical in EBV pathogenesis, understanding the mechanisms that underpin EBV regulation of apoptosis therefore provides opportunities for novel therapeutic interventions.

Details

Original languageEnglish
JournalViruses
Volume9
Issue number11
Publication statusPublished - 13 Nov 2017

Keywords

  • Journal Article, Review, EBV , apoptosis , genetic cooperation , latency , virus cancers , p53 , BCL-2 family , growth transformation