Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis

Int J Biol Sci. 2016 Oct 18;12(11):1309-1318. doi: 10.7150/ijbs.16564. eCollection 2016.

Abstract

Epstein-Barr virus (EBV) has been associated with several types of human cancers. In the host, EBV can establish two alternative modes of life cycle, known as latent or lytic and the switch from latency to the lytic cycle is known as EBV reactivation. Although EBV in cancer cells is found mostly in latency, a small number of lytically-infected cells promote carcinogenesis through the release of growth factors and oncogenic cytokines. This review focuses on the mechanisms by which EBV reactivation is controlled by cellular and viral factors, and discusses how EBV lytic infection contributes to human malignancies.

Keywords: Epstein-Barr virus; Rta; Zta; carcinogenesis; latency; reactivation.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinogenesis / pathology
  • DNA Methylation / genetics
  • Epigenesis, Genetic / genetics
  • Epstein-Barr Virus Infections / complications*
  • Epstein-Barr Virus Infections / metabolism
  • Herpesvirus 4, Human / pathogenicity
  • Humans
  • Immediate-Early Proteins / metabolism
  • Oxidative Stress / genetics
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • Trans-Activators / metabolism

Substances

  • BZLF1 protein, Herpesvirus 4, Human
  • IE2 protein, bovine herpesvirus type 4
  • Immediate-Early Proteins
  • Trans-Activators