Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript-Reference-Cited by-同舟云学术

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

Published:2000-02-25 Issue:5457 Volume:287 Page:1500-1503
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Perng Guey-Chuen¹,Jones Clinton²,Ciacci-Zanella Janice²,Stone Melissa²,Henderson Gail²,Yukht Ada¹,Slanina Susan M.¹,Hofman Florence M.,Ghiasi Homayon¹³,Nesburn Anthony B.¹³,Wechsler Steven L.¹³

Affiliation:

1. Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns & Allen Research Institute, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.

2. Department of Veterinary and Biomedical Sciences, Center for Biotechnology, University of Nebraska, Lincoln, NE 68583, USA. 3Department of Pathology, University of Southern California School of Medicine, Los Angeles, CA 90025, USA.

3. Department of Ophthalmology, UCLA School of Medicine, Los Angeles, CA 90024, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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