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J Virol. 2017 Jan 3;91(2). pii: e01419-16. doi: 10.1128/JVI.01419-16. Print 2017 Jan 15.

Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation.

Author information

1
Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA.
2
Department of Microbiology, New York University School of Medicine, New York, New York, USA angus.wilson@med.nyu.edu.

Abstract

Herpes simplex virus (HSV) establishes a latent reservoir in neurons of human peripheral nerves. In this quiescent state, the viral genome persists as a circular, histone-associated episome, and transcription of viral lytic cycle genes is largely suppressed through epigenetic processes. Periodically, latent virus undergoes reactivation whereby lytic genes are activated and viral replication occurs. In this Gem, we review recent evidence that mechanisms governing the initial transcription of lytic genes are distinct from those of de novo infection and directly link reactivation to neuronal stress response pathways. We also discuss evidence that lytic cycle gene expression can be uncoupled from the full reactivation program, arguing for a less sharply bimodal definition of latency.

KEYWORDS:

JNK signaling; episome; herpes simplex virus; heterochromatin; histone methylation; latency; neurotropic viruses; reactivation; transcriptional regulation

PMID:
27807236
PMCID:
PMC5215350
DOI:
10.1128/JVI.01419-16
[Indexed for MEDLINE]
Free PMC Article

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