| Literature DB >> 10688801 |
G C Perng1, C Jones, J Ciacci-Zanella, M Stone, G Henderson, A Yukht, S M Slanina, F M Hofman, H Ghiasi, A B Nesburn, S L Wechsler.
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.Entities:
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Year: 2000 PMID: 10688801 DOI: 10.1126/science.287.5457.1500
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728