在αherpesvirus从神经元退出期间,gE/gI复合物对于激素-1的招募是必要的
Drishya Diwaker1, DongHo Kim2, Dylann Cordova-Martinez3
1Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, New York, New York, USA.
Journal of virology
|December 9, 2024
概括
阿尔法疹病毒的输出依赖于gE/gI-US9p复杂的协调动力发动机. 这个复合体指导沿神经元轴突进行病毒颗粒运输以进行传播和感染.
科学领域:
- 神经病毒学 神经病毒学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 阿尔法疹病毒在周围神经系统中建立终身潜伏感染.
- 在重新激活后,病毒从神经元扩散到上皮细胞,引起疾病.
- 来自神经元的病毒输出涉及沿轴突运输,这一过程尚未完全理解.
研究的目的:
- 阐明alphaherpesvirus协调前进轴突运输的动力活动的机制.
- 研究病毒gE/gI-US9p复合体在神经元退出过程中招募和协调激素运动器的作用.
主要方法:
- 在差异化的CAD神经元和背根 (DRG) 感觉神经元中利用伪狂犬病病毒 (PRV).
- 通过同局部化研究和依赖性测试,研究了蛋白质与蛋白质相互作用.
- 通过微管过乙化 (三氨酸A,图巴) 操纵了kinesin-1运动活性.
主要成果:
- PRV输出涉及kinesin-3 (KIF1A) 和神经元kinesin-1 (KIF5A/C) 电机,但不是KIF5B.
- KIF1A的招聘取决于US9p,而KIF5的招聘需要gE/gI.
- 增强的kinesin-1活性增加了PRV粒子在轴突中的贩运,这取决于gE/gI.
结论:
- 该gE/gI-US9p复合体在alphaherpesvirus轴突传输过程中起到关键作用,作为激素电机的协调者.
- 首先由US9p招募KIF1A,然后通过gE/gI介导招募KIF5A/C,以实现高效的轴突运输.
- 这种协调的运动活动有助于病毒的传播和复发性感染.
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