PDF(Pubmed)
Abstract：
The maintenance of viral protein homeostasis depends on the interaction between host cell proteins and viral proteins. As a molecular chaperone, heat shock protein 70 (HSP70) has been shown to play an important role in viral infection. Our results showed that HSP70 can affect translation, replication, assembly, and release during the life cycle of duck hepatitis A virus type 1 (DHAV-1). We demonstrated that HSP70 can regulate viral translation by interacting with the DHAV-1 internal ribosome entry site (IRES). In addition, HSP70 interacts with the viral capsid proteins VP1 and VP3 and promotes their stability by inhibiting proteasomal degradation, thereby facilitating the assembly of DHAV-1 virions. This study demonstrates the specific role of HSP70 in regulating DHAV-1 replication, which are helpful for understanding the pathogenesis of DHAV-1 infection and provide additional information about the role of HSP70 in infection by different kinds of picornaviruses, as well as the interaction between picornaviruses and host cells.
摘要：
病毒蛋白稳态的维持取决于宿主细胞蛋白和病毒蛋白之间的相互作用。作为分子伴侣,热休克蛋白70（HSP70）已被证明在病毒感染中起重要作用。我们的结果表明，HSP70可以影响翻译，复制,装配,并在鸭甲型肝炎病毒1型（DHAV-1）的生命周期中释放。我们证明HSP70可以通过与DHAV-1内部核糖体进入位点（IRES）相互作用来调节病毒翻译。此外,HSP70与病毒衣壳蛋白VP1和VP3相互作用，并通过抑制蛋白酶体降解促进其稳定性，从而促进DHAV-1病毒体的组装。这项研究证明了HSP70在调节DHAV-1复制中的特定作用，这有助于了解DHAV-1感染的发病机理，并提供有关HSP70在不同种类的小核糖核酸病毒感染中的作用的其他信息，以及微小核糖核酸病毒和宿主细胞之间的相互作用。
