Abdel-Latif Lubna, Murray Byron K, Renberg Rebecca L, O'Neill Kim L, Porter Heidi, Jensen James B, Johnson F Brent
Department of Microbiology and Molecular Biology, Brigham Young University, 887 WIDB, Provo, UT 84602, USA.
J Gen Virol. 2006 Sep;87(Pt 9):2539-2548. doi: 10.1099/vir.0.81915-0.
The helper-independent bovine parvovirus (BPV) was studied to determine its effect on host embryonic bovine tracheal (EBTr) cells: whether the ultimate outcome of infection results in apoptotic cell death or cell death by necrosis. Infected cells were observed for changes marking apoptosis. Observations of alterations in nuclear morphology, membrane changes, apoptotic body formation, membrane phosphatidylserine inversions, caspase activation and cell DNA laddering in infected cells were not indicative of apoptosis. On the other hand, at the end of the virus replication cycle, infected cells released viral haemagglutinin and infectious virus particles, as would be expected from cell membrane failure. Moreover, the infected cells released lactate dehydrogenase (LDH), release of which is a marker of necrosis. LDH release into the cell medium correlated directly with viral m.o.i. and time post-infection. Furthermore, assessment of mitochondrial dehydrogenase activity was consistent with cell death by necrosis. Taken together, these findings indicate that cell death in BPV-infected EBTr cells is due to necrosis, as defined by infected-cell membrane failure and release of the cell contents into the extracellular environment.
对非依赖辅助病毒的牛细小病毒（BPV）进行了研究，以确定其对宿主胚胎牛气管（EBTr）细胞的影响：感染的最终结果是导致细胞凋亡死亡还是坏死性细胞死亡。观察感染细胞中标志凋亡的变化。对感染细胞中核形态改变、膜变化、凋亡小体形成、膜磷脂酰丝氨酸外翻、半胱天冬酶激活和细胞DNA梯状条带的观察并不表明存在凋亡。另一方面，在病毒复制周期结束时，感染细胞释放病毒血凝素和传染性病毒颗粒，这正如细胞膜功能衰竭所预期的那样。此外，感染细胞释放乳酸脱氢酶（LDH），其释放是坏死的一个标志。LDH释放到细胞培养基中与病毒感染复数和感染后时间直接相关。此外，线粒体脱氢酶活性的评估与坏死性细胞死亡一致。综上所述，这些发现表明，BPV感染的EBTr细胞中的细胞死亡是由于坏死，这是由感染细胞膜功能衰竭以及细胞内容物释放到细胞外环境所定义的。
