Department of Virology, Graduate School of Medicine, Nagoya University, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8560, Japan.
Arch Virol. 2010 Aug;155(8):1235-45. doi: 10.1007/s00705-010-0712-2. Epub 2010 Jun 11.
We compared apoptosis induction in mice following three routes of infection. After intravenous infection, wild-type herpes simplex virus (HSV) types 1 and 2 and US3Delta mutants infected the adrenal gland and caused apoptosis. Corneal infection with wild-type virus resulted in apoptosis in a fraction of infected epithelium cells. Interestingly, many uninfected cells were apoptotic in the retina. Although neurons in the trigeminal ganglion were heavily infected, no apoptotic neurons were observed. Intracranial infection with wild-type virus resulted in HSV-infected cells inside the brain; however, most of the infected neurons escaped apoptosis. In contrast, infection with US3Delta and gamma(1)34.5Delta mutants caused apoptosis in infected neurons. Cleaved caspase-8 and p53 were detected in apoptotic cells in the adrenal gland and the brain; however, phospho-JNK was detected only in apoptotic cells of the brain. These results suggest that the activation of apoptotic signaling proteins differs depending on the host cell type and modulates the induction of apoptosis in HSV-infected cells.
我们比较了三种感染途径后小鼠的细胞凋亡诱导情况。静脉感染后，野生型单纯疱疹病毒 (HSV) 1 型和 2 型和 US3Delta 突变体感染肾上腺并引起细胞凋亡。角膜感染野生型病毒导致部分感染上皮细胞发生细胞凋亡。有趣的是，在视网膜中有许多未感染的细胞发生凋亡。尽管三叉神经节中的神经元受到严重感染，但未观察到凋亡神经元。颅内感染野生型病毒导致大脑内有 HSV 感染细胞；然而，大多数感染的神经元逃脱了凋亡。相比之下，感染 US3Delta 和 gamma(1)34.5Delta 突变体导致感染神经元发生细胞凋亡。在肾上腺和大脑中的凋亡细胞中检测到裂解的 caspase-8 和 p53；然而，仅在大脑中的凋亡细胞中检测到磷酸化 JNK。这些结果表明，凋亡信号蛋白的激活取决于宿主细胞类型，并调节 HSV 感染细胞的凋亡诱导。
