Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript
Guey‐Chuen Perng(Cedars-Sinai Medical Center), Clinton Jones(University of Nebraska–Lincoln), J. R. C. Zanella(University of Nebraska–Lincoln), Melissa Stone(University of Nebraska–Lincoln), Gail Henderson(University of Nebraska–Lincoln), Ada Yukht(Cedars-Sinai Medical Center), Susan M. Slanina(Cedars-Sinai Medical Center), Florence M. Hofman(University of Southern California), Homayon Ghiasi(Cedars-Sinai Medical Center), Anthony B. Nesburn(Cedars-Sinai Medical Center), Steven L. Wechsler(Cedars-Sinai Medical Center)
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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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