Department of Cell Biology, University of São Paulo School of Medicine at Ribeirão Preto, Av. dos Bandeirantes, 3900, 14049-900, SP, Brazil.
Virology. 2010 Jan 20;396(2):256-63. doi: 10.1016/j.virol.2009.10.005. Epub 2009 Nov 10.
Coxsackievirus B5 (CVB5), a human enterovirus of the family Picornaviridae, is a frequent cause of acute and chronic human diseases. The pathogenesis of enteroviral infections is not completely understood, and the fate of the CVB5-infected cell has a pivotal role in this process. We have investigated the CVB5-induced apoptosis of HeLa cells and found that it happens by the intrinsic pathway by a mechanism dependent on the ubiquitin-proteasome system, associated with nuclear aggregation of p53. Striking redistribution of both SUMO and UBC9 was noted at 4 h post-infection, simultaneously with a reduction in the levels of the ubiquitin-ligase HDM2. Taken together, these results suggest that CVB5 infection of HeLa cells elicit the intrinsic pathway of apoptosis by MDM2 degradation and p53 activation, destabilizing protein sumoylation, by a mechanism that is dependent on a functional ubiquitin-proteasome system.
柯萨奇病毒 B5(CVB5)是小核糖核酸病毒科的一种人类肠道病毒,是引起急性和慢性人类疾病的常见原因。肠道病毒感染的发病机制尚不完全清楚,而 CVB5 感染细胞的命运在这一过程中起着关键作用。我们研究了 CVB5 诱导的 HeLa 细胞凋亡,发现它通过依赖泛素蛋白酶体系统的内在途径发生,与 p53 的核聚集有关。在感染后 4 小时,注意到 SUMO 和 UBC9 的明显重新分布,同时泛素连接酶 HDM2 的水平降低。综上所述,这些结果表明,CVB5 感染 HeLa 细胞通过 MDM2 降解和 p53 激活诱导内在凋亡途径,通过一种依赖功能泛素蛋白酶体系统的机制破坏蛋白质 SUMO 化。