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Gem

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

Anna R. Cliffe, Angus C. Wilson
Felicia Goodrum, Editor
Anna R. Cliffe
aDepartment of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA
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Angus C. Wilson
bDepartment of Microbiology, New York University School of Medicine, New York, New York, USA
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Felicia Goodrum
University of Arizona
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DOI: 10.1128/JVI.01419-16
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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.

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Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation
Anna R. Cliffe, Angus C. Wilson
Journal of Virology Jan 2017, 91 (2) e01419-16; DOI: 10.1128/JVI.01419-16

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Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation
Anna R. Cliffe, Angus C. Wilson
Journal of Virology Jan 2017, 91 (2) e01419-16; DOI: 10.1128/JVI.01419-16
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  • Article
    • ABSTRACT
    • INTRODUCTION
    • WHAT IS LATENCY?
    • MECHANISMS OF HSV LYTIC GENE EXPRESSION DURING THE FIRST PHASE OF HSV REACTIVATION ARE DISTINCT FROM THOSE OF DE NOVO INFECTION
    • CO-OPTION OF A NEURONAL STRESS PATHWAY FOR PHASE I OF REACTIVATION
    • THE SECOND PHASE OF REACTIVATION CLOSELY RESEMBLES DE NOVO INFECTION
    • LATENT INFECTION IN VIVO IS DYNAMIC
    • CONCLUSIONS AND FUTURE DIRECTIONS
    • REFERENCES
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KEYWORDS

Gene Expression Regulation, Viral
herpes simplex
Simplexvirus
Transcription, Genetic
Virus Activation
virus replication
JNK signaling
episome
herpes simplex virus
heterochromatin
histone methylation
latency
neurotropic viruses
reactivation
transcriptional regulation

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