Regulation of the latent-lytic switch in Epstein-Barr virus

Semin Cancer Biol. 2014 Jun;26:60-8. doi: 10.1016/j.semcancer.2014.01.002. Epub 2014 Jan 20.

Abstract

Epstein-Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically.

Keywords: Ataxia-telangiectasia mutated (ATM); Genome methylation; Hypoxia; Lytic induction therapy; TGF-β.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • DNA Methylation
  • Epstein-Barr Virus Infections / virology*
  • Gene Expression Regulation, Viral
  • Genome, Viral
  • Herpesvirus 4, Human / physiology*
  • Humans
  • Neoplasms / therapy
  • Neoplasms / virology
  • Oncolytic Virotherapy
  • Oncolytic Viruses / physiology
  • Virus Activation
  • Virus Latency*
  • Virus Replication*