Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript

Authors

Guey-Chuen Perng, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA
Clinton J. Jones, University of Nebraska - LincolnFollow
Janice Ciacci-Zanella, University of Nebraska - Lincoln
Melissa Stone, University of Nebraska - Lincoln
Gail A. Henderson, University of Nebraska - LincolnFollow
Ada Yukht, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA
Susan M. Slanina, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA
Florence M. Hofman, University of Southern California School of Medicine, Los Angeles, CA
Homayon Ghiasi, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA
Anthony B. Nesburn, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA
Steven L. Wechsler, Ophthalmology Research Laboratories, Cedars-Sinai, Medical Center Burns & Allen Research Institute, Los Angeles, CA

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.