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Autophagy. 2016;12(3):451-9. doi: 10.1080/15548627.2016.1139262. Epub 2016 Mar 2.

Autophagy interaction with herpes simplex virus type-1 infection.

Author information

1
a Department of Molecular Microbiology and Immunology , Keck Medical School, University of Southern California , Los Angeles , CA , USA.

Abstract

More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.

KEYWORDS:

ICP34.5; autophagy; herpes simplex virus; immune evasion; neurodegeneration

PMID:
26934628
PMCID:
PMC4836034
[Available on 2017-03-02]
DOI:
10.1080/15548627.2016.1139262
[Indexed for MEDLINE]
Free PMC Article

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