小RNA病毒致病机理的研究  

Study on the Pathogenesis of Picornaviruses

作　　者：张峰[1,2] 张瑜[1] 王树瑜[1] 张勇[1] 

机构地区：[1]甘肃农业大学动物医学院,甘肃兰州730070 [2]中农威特生物科技股份有限公司,甘肃兰州730046

出　　处：《安徽农业科学》2013年第23期9541-9543,共3页Journal of Anhui Agricultural Sciences

基　　金：甘肃省生物技术专项

摘　　要：很多小RNA科病毒感染宿主细胞后可通过自身的核酸序列或病毒性蛋白产物控制靶细胞的生命活动,而被感染细胞也会通过自身的调控机制对侵染的病毒进行有限的反击,这种现象被认为是宿主细胞对抗小RNA科病毒侵染的防御机制。这种侵染与抵抗的互作机制可由某些病毒蛋白对细胞产生信号干扰或细胞自身翻译合成的细胞因子对病毒的复制路径进行封堵来实现。虽然这些信号通路的上游事件是不同的,但最后的效应却很统一,即使细胞崩解或者细胞将自身按照一定程序与所侵入的病毒同归于尽。此外,一些病毒蛋白具有抑制细胞程序性自杀的功能,它们能够令感染病毒后的细胞不死亡,形成病毒与宿主细胞共存的持续性感染状态。Many RNA viruses could control the life actions of the target cells by self nucleotide sequences or viral protein products after infecting the host ceils. And the infected ceils could beat back limitedly on the infecting viruses by their own regulation system. The phenomenon was re- garded as the defense mechanism of host ceils against the infection of picornaviruses. The interaction mechanism between infection and resistance could be realized by signal interference of some viral proteins to cells or the plug of virus copy path by the cell factors that were translated and synthesized by cells. Though the upstream events of these signal pathways were different, but the final effects that made cell collapse or suicide with the infecting virus were consistent. In addition, some viral proteins could suppress the cell programmed death and inhibit the cell death after virus infection to form the persistent infection with the coexistence between viruses and host cells.

关 键 词：小RNA病毒 病毒性蛋白产物 细胞因子 持续性感染 

分 类 号：S852.65[农业科学—基础兽医学]