Akabane病毒重编程PKR-eIf2α-SGs/PBs轴以精细调控帽捕获效率
Zhongyin Liu1, Dongjie Chen2, Jiamin Qin1
1Beijing Key Laboratory of Traditional Chinese Veterinary Medicine, College of Veterinary Medicine, Beijing University of Agriculture, Beijing, China.
Virulence
|October 12, 2026
Abstract:
Akabane病毒(AKAV)通过“抢帽”机制在细胞质中启动转录。细胞质中的宿主mRNA是主要的帽供体,但其亚细胞定位对抢帽过程的影响尚不清楚。本文中,我们证明AKAV诱导多聚核糖体、应激颗粒(SGs)和加工小体(PBs)的解聚,共同促进病毒的抢帽过程。从机制上讲,AKAV感染激活PKR-eIF2α信号通路,导致多聚核糖体解聚并引发翻译关闭。有趣的是,病毒N蛋白通过与这些颗粒中被隔离的RNA竞争,从而解聚SGs和PBs,而其RNA结合残基的突变则会消除该功能。此外,抑制PKR-eIF2α通路会损害AKAV的复制和抢帽效率。而通过G3BP1敲低或化学试剂抑制SGs则显著增强病毒复制和抢帽效率,表明多聚核糖体和SGs的解聚有利于帽的获取。另外,N蛋白介导的PBs解聚可保护mRNA免于降解,抑制PBs亦可增强抢帽效率。综上所述,AKAV已进化出一种复杂策略,通过重编程mRNA的分布,创造有利于病毒抢帽的细胞环境。
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