Veterinary and Biomedical Sciences, Department of

 

Document Type

Article

Date of this Version

February 2000

Comments

Published in SCIENCE 25 FEBRUARY 2000, VOL 287. Copyright 2000. Used by permission. Online at www.sciencemag.org

Abstract

Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT- virus but not with LAT+ viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells. Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.

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