参与EV71复制的宿主因素hnRNP K、RTN3的分子作用机制研究进展

Molecular Mechanism of Action of hnRNP K and RTN3 in the Replication of Enterovirus 71

肠道病毒71(Enterovirus 71,EV71)是引发儿童重症手足口病的主要致病病原体之一,其在人体细胞内发生复制的具体分子机制目前还尚不明确。最近研究发现,一些宿主因素参与了EV71的复制,如核不均一核糖核蛋白K(Heterogeneous nuclear ribonucleoprotein K,hnRNP K)以及网状蛋白3(Reticulon3,RTN3)。在这些发现中,有学者通过竞争性实验证实,hnRNP K与EV71 5′UTR间能够相互作用,并在病毒RNA的有效合成中是必不可少的;另外一些学者采用酵母双杂交系统等实验发现,RTN3可与EV71 2CN端区域相互作用,并在EV71的复制过程中起着非常关键的作用。本文将主要围绕这些研究,综述hnRNP K及RTN3在EV71复制中的相关分子作用机制。

Enterovirus 71（EV71）is a neurotropic pathogen that can induce hand,foot and mouth disease in children.There is an appreciable mortality rate after EV71 infections.The mechanism of action of EV71 replication is not known.Recent work has identified some of cell factors of the host that participate in the synthesis of the RNA and proteins of EV71（e.g.,hnRNP K,reticulon 3（RTN 3））.In that work,researchers used a competitive assay to show that hnRNP K can interact with EV71 5′UTR,which is required for efficient synthesis of viral RNA.Using ayeast two-hybrid system,other researchers demonstrated that RTN 3interacts with the N-terminal domain of EV71 2C,which is crucial for replication of viral RNA.Here,we discuss recent work focusing on the molecular mechanisms of hnRNP K and RTN 3in the synthesis of the RNA and proteins of EV71.