Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript

被引:351
作者
Perng, GC
Jones, C
Ciacci-Zanella, J
Stone, M
Henderson, G
Yukht, A
Slanina, SM
Hofman, FM
Ghiasi, H
Nesburn, AB
Wechsler, SL
机构
[1] Cedars Sinai Med Ctr, Burns & Allen Res Inst, Ophthalmol Res Labs, Los Angeles, CA 90048 USA
[2] Univ Nebraska, Ctr Biotechnol, Dept Vet & Biomed Sci, Lincoln, NE 68583 USA
[3] Univ Calif Los Angeles, Sch Med, Dept Pathol, Los Angeles, CA 90025 USA
[4] Univ Calif Los Angeles, Sch Med, Dept Ophthalmol, Los Angeles, CA 90024 USA
关键词
D O I
10.1126/science.287.5457.1500
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1500 / 1503
页数:4
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