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肠道病毒D68 2A蛋白酶导致核毛孔复合物的功能障碍和运动神经元毒性

Katrina M Zinn, Mathew W McLaren, Michael T Imai

bioRxiv : the preprint server for biology

|February 20, 2025

概括

肠道病毒D68蛋白酶破坏核毛孔综合体 (NPC),导致急性软性髓炎 (AFM) 中的运动神经元死亡. 准这些蛋白酶可能为AFM提供新的治疗策略.

科学领域:

病毒学病毒学
神经科学是一个神经科学.
细胞生物学细胞生物学

背景情况:

肠道病毒D68 (EV-D68) 导致急性软骨髓炎 (AFM),其特征是运动神经元死亡.
关联EV-D68与神经毒性,特别是运动神经元损伤的机制尚不清楚.
核孔综合体 (NPC) 功能障碍与神经退行性疾病有关,并在皮科纳病毒感染期间发生变化.

研究的目的:

研究EV-D68蛋白酶对NPC结构和功能的影响.
确定EV-D68蛋白酶在运动神经元毒性的作用.

主要方法:

在EV-D68蛋白酶表达后对NPC组成的分析.
使用报告员系统来评估NPC功能 (核进出口,透性).
在诱导的多能干细胞衍生的运动神经元中评估了毒性,并测试了一种蛋白酶抑制剂.

主要成果:

EV-D68 2A 和 3C 蛋白酶通过 2Apro. 分裂关键核波林,包括 Nup98 和 POM121.
2Apro抑制了核进出口,并破坏了NPC的透性,但没有影响RNA的出口.
2Apro对运动神经元有毒,在亚抗病毒度下,telaprevir可以挽救毒性.

结论:

EV-D68蛋白酶,特别是2Apro,显著破坏NPC的完整性和功能.
由EV-D68蛋白酶介导的NPC功能障碍有助于AFM中运动神经元毒性.
准EV-D68蛋白酶或NPC为AFM提供了一个潜在的治疗途径.

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