在EV-D68感染期间诱导的线细胞促进病毒非解毒释放
Alagie Jassey1, Bimal Paudel1, Michael A Wagner1
1Department of Microbiology and Immunology and Center for Pathogen Research, University of Maryland School of Medicine, 685 W. Baltimore Avenue, Baltimore, MD 21201, USA.
bioRxiv : the preprint server for biology
|December 16, 2024
概括
肠道病毒-D68 (EV-D68) 劫持了线粒体的选择性降解,以促进其从宿主细胞释放. 这一过程对于非溶性肠道病毒的释放至关重要.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 自学研究 自学研究
背景情况:
- 肠道病毒-D68 (EV-D68) 引起呼吸道感染和罕见的急性软骨髓炎.
- EV-D68使用非选择性自为复制.
- 特定的自途径在EV-D68释放中的作用尚不清楚.
研究的目的:
- 为了调查EV-D68是否会诱导线粒.
- 为了确定由EV-D68.8.诱导线粒细胞衰变的机制.
- 为了阐明 mitophagy 在 EV-D68 释放中的作用.
主要方法:
- 细胞感染了EV-D68.8. 的细胞.
- 显微镜观察菌的标志 (线粒体碎片化,帕金斯转位).
- 病毒RNA复制和释放的分析.
- 线粒细胞衰变信号元件的消耗.
主要成果:
- EV-D68感染诱导了线粒,包括线粒细胞的形成和线粒体的分裂.
- EV-D68 3C蛋白酶分裂了线粒体素-2,导致线粒体的分裂.
- 碎片化的线粒体与病毒RNA局部化.
- 线粒细胞衰竭减少了EV-D68的释放,但没有影响细胞内病毒标位.
结论:
- EV-D68通过线粒素-2的蛋白酶分裂诱导线粒细胞衰变.
- 线性会调节感染细胞中EV-D68的非性释放.
- 虽然大自能支持EV-D68的复制,但小自能特别控制其释放.
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