Epigenetic crossroads of the Epstein-Barr virus B-cell relationship

Curr Opin Virol. 2018 Oct:32:15-23. doi: 10.1016/j.coviro.2018.08.012. Epub 2018 Sep 15.

Abstract

Epstein-Barr virus (EBV) is a gamma-herpesvirus that establishes lifelong infection in the majority of people worldwide. EBV uses epigenetic reprogramming to switch between multiple latency states in order to colonize the memory B-cell compartment and to then periodically undergo lytic reactivation upon plasma cell differentiation. This review focuses on recent advances in the understanding of epigenetic mechanisms that EBV uses to control its lifecycle and to subvert the growth and survival pathways that underly EBV-driven B-cell differentiation versus B-cell growth transformation, a hallmark of the first human tumor virus. These include the formation of viral super enhancers that drive expression of key host dependency factors, evasion of tumor suppressor responses, prevention of plasmablast differentiation, and regulation of the B-cell lytic switch.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / cytology
  • B-Lymphocytes / virology*
  • Cell Differentiation
  • Epigenesis, Genetic*
  • Epstein-Barr Virus Infections / virology
  • Gene Expression Regulation, Viral
  • Herpesvirus 4, Human / genetics*
  • Herpesvirus 4, Human / physiology
  • Host-Pathogen Interactions
  • Humans
  • Mice
  • Virus Latency / genetics*