Department of Pediatrics and Center for Infectious Diseases and Microbiology Translational Research, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
J Virol. 2010 Mar;84(6):3116-20. doi: 10.1128/JVI.01726-09. Epub 2010 Jan 13.
Herpes simplex virus type 2 (HSV-2) induces apoptosis in T cells by a caspase-dependent mechanism. Apoptosis can occur via extrinsic (death receptor) and/or intrinsic (mitochondrial) pathways. Here, we show that the initiator caspase for the intrinsic pathway is activated in T cells following HSV-2 exposure. To determine the respective contributions of intrinsic and extrinsic pathways, we assessed apoptosis in Jurkat cells that are deficient in caspase 8 or Fas-associating protein with death domain (FADD) for the extrinsic pathway and in cells deficient in caspase 9 for the intrinsic pathway. Our results indicate HSV-2-induced apoptosis in T cells occurs via the intrinsic pathway.
单纯疱疹病毒 2 型（HSV-2）通过半胱天冬酶依赖性机制诱导 T 细胞凋亡。凋亡可通过外在（死亡受体）和/或内在（线粒体）途径发生。在这里，我们表明 T 细胞在 HSV-2 暴露后，内在途径的起始半胱天冬酶被激活。为了确定内在和外在途径的各自贡献，我们评估了缺乏外在途径的半胱天冬酶 8 或 Fas 相关死亡结构域蛋白（FADD）的 Jurkat 细胞以及内在途径中缺乏半胱天冬酶 9 的细胞中的凋亡。我们的结果表明，HSV-2 诱导的 T 细胞凋亡是通过内在途径发生的。
