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Science 25 February 2000:
Vol. 287. no. 5457, pp. 1500 - 1503
DOI: 10.1126/science.287.5457.1500
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Reports

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

Guey-Chuen Perng, 1 Clinton Jones, 2 Janice Ciacci-Zanella, 2 Melissa Stone, 2 Gail Henderson, 2 Ada Yukht, 1 Susan M. Slanina, 1 Florence M. Hofman, Homayon Ghiasi, 14 Anthony B. Nesburn, 14 Steven L. Wechsler 14*

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.

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.
4 Department of Ophthalmology, UCLA School of Medicine, Los Angeles, CA 90024, USA.
*   To whom correspondence should be addressed. E-mail: Wechsler{at}CSMC.edu

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