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

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

Author information

1
Graduate Program in Virology, Harvard Medical School, Boston, MA, 02115, USA.
2
Graduate Program in Virology, Harvard Medical School, Boston, MA, 02115, USA; Division of Infectious Disease, Department of Medicine, Brigham & Women's Hospital, Boston, MA, 02115, USA; Department of Microbiology, Harvard Medical School, Boston, MA, 02115, USA; Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, 02142, USA. Electronic address: bgewurz@bwh.harvard.edu.

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.

PMID:
30227386
PMCID:
PMC6263794
[Available on 2019-10-01]
DOI:
10.1016/j.coviro.2018.08.012

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