当前位置: X-MOL 学术Virology › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Expression of flavivirus capsids enhance the cellular environment for viral replication by activating Akt-signalling pathways
Virology ( IF 3.7 ) Pub Date : 2018-01-19 , DOI: 10.1016/j.virol.2018.01.009
Adriana M. Airo , Matt D. Urbanowski , Joaquin Lopez-Orozco , Jae Hwan You , Tamara D. Skene-Arnold , Charles Holmes , Vladimir Yamshchikov , Natasha Malik-Soni , Lori Frappier , Tom C. Hobman

Flaviviruses depend on multiple host pathways during their life cycles and have evolved strategies to avoid the innate immune response. Previously, we showed that the West Nile virus capsid protein plays a role in this process by blocking apoptosis. In this study, we examined how expression of capsid proteins from several flaviviruses affects apoptosis and other host processes that impact virus replication. All of the tested capsid proteins protected cells from Fas-dependent apoptosis through a mechanism that requires activated Akt. Capsid expression upregulated other Akt-dependent cellular processes including expression of glucose transporter 1 and mitochondrial metabolism. Protein phosphatase 1, which is known to inactivate Akt, was identified as a DENV capsid interacting protein. This suggests that DENV capsid expression activates Akt by sequestering phosphatases that downregulate phospho-Akt. Capsid-dependent upregulation of Akt would enhance downstream signalling pathways that affect cell survival and metabolism, thus providing a favourable environment for virus replication.



中文翻译:

黄病毒衣壳的表达通过激活Akt信号通路增强了病毒复制的细胞环境

黄病毒在其生命周期中依赖于多种宿主途径,并已发展出避免先天免疫反应的策略。以前,我们证明了西尼罗河病毒衣壳蛋白通过阻止细胞凋亡在此过程中发挥作用。在这项研究中,我们检查了几种黄病毒中衣壳蛋白的表达如何影响细胞凋亡以及其他影响病毒复制的宿主过程。所有测试的衣壳蛋白均通过需要激活Akt的机制保护细胞免受Fas依赖性细胞凋亡的影响。衣壳表达上调了其他依赖Akt的细胞过程,包括葡萄糖转运蛋白1的表达和线粒体代谢。蛋白磷酸酶1(已知可灭活Akt)被鉴定为DENV衣壳相互作用蛋白。这表明DENV衣壳表达通过螯合下调磷酸化Akt的磷酸酶来激活Akt。衣壳依赖的Akt上调会增强影响细胞存活和代谢的下游信号传导途径,从而为病毒复制提供有利的环境。

更新日期:2018-01-19
down
wechat
bug