Department of Microbiology and Plant Pathology, University of Pretoria, Pretoria 0002, South Africa.
Virus Res. 2012 Jan;163(1):385-9. doi: 10.1016/j.virusres.2011.09.033. Epub 2011 Sep 29.
Infection of mammalian cell cultures with African horse sickness virus (AHSV) is known to result in dramatic cytopathic effects (CPE), but no CPE is observed in infected insect cell cultures despite productive virus replication. The basis for this phenomenon has not yet been investigated, but is suggestive of apoptosis being induced following virus infection of the mammalian cells. To investigate whether AHSV can induce apoptosis in infected mammalian cells, Culicoides variipennis (KC) insect cells and BHK-21 mammalian cells were infected with AHSV-9 and analyzed for morphological and biochemical hallmarks of apoptosis. In contrast to KC cells, infection of BHK-21 cells with AHSV-9 resulted in ultrastructural changes and nuclear DNA fragmentation, both of which are associated with the induction of apoptosis. Results also indicated that AHSV-9 infection of BHK-21 cells resulted in activation of caspase-3, a key agent in apoptosis, and in mitochondrial membrane depolarization. Cumulatively, the data indicate that the intrinsic pathway is activated in AHSV-induced apoptosis.
哺乳动物细胞培养物感染非洲马瘟病毒（AHSV）已知会导致明显的细胞病变效应（CPE），但在感染昆虫细胞培养物中观察不到 CPE，尽管病毒复制具有生产性。尚未研究这种现象的基础，但提示哺乳动物细胞感染病毒后会诱导细胞凋亡。为了研究 AHSV 是否可以在感染的哺乳动物细胞中诱导细胞凋亡，用 AHSV-9 感染了库蠓（KC）昆虫细胞和 BHK-21 哺乳动物细胞，并分析了凋亡的形态学和生化特征。与 KC 细胞相反，用 AHSV-9 感染 BHK-21 细胞会导致超微结构变化和核 DNA 片段化，这两者都与细胞凋亡的诱导有关。结果还表明，AHSV-9 感染 BHK-21 细胞会导致半胱天冬酶-3（凋亡的关键因子）的激活以及线粒体膜去极化。总的来说，这些数据表明，内在途径在 AHSV 诱导的凋亡中被激活。
