HSV LAT and neuronal survival.

Abstract:

:Herpes Simplex Virus (HSV) establishes a latent infection within sensory neurons and periodically reactivates in response to stress. HSV's ability to inhabit neurons for the life of the host involves a number of virally encoded functions that tightly regulate the latency-reactivation cycle, preventing uncontrolled spread of reactivating virus and large-scale death of neurons. The HSV latency-associated transcript (LAT) is a complex transcription unit expressed primarily in neurons containing latent genomes. While mutational analyses indicate LAT is nonessential for viral replication, the 5' exon of LAT greatly enhances reactivation. Several studies have also identified LAT mutations that reduce establishment of latency and enhance virulence. Recently, LAT has also been shown to inhibit cell death through by blocking caspase-8 and caspase-9 pathways. While blocking apoptosis is not essential for either establishment of latency or reactivation, it likely augments these processes and may contribute to HSV's long-term persistence and spread.

journal_name

Int Rev Immunol

authors

Bloom DC

doi

10.1080/08830180490265592

subject

Has Abstract

pub_date

2004-01-01 00:00:00

pages

187-98

issue

1-2

eissn

0883-0185

issn

1563-5244

pii

PBD572D6DK8N3TUN

journal_volume

23

pub_type

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