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Updated: Sep 11, 2025

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纽卡斯尔病病毒利用脂翻酶ATP11c-CDC50A复合体促进病毒感染
Dandan Zhang1, Yuechi Hou2, Xusheng Qiu1
1Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, China.
The Journal of biological chemistry
|August 14, 2025
概括
纽卡斯尔病病毒 (NDV) 劫持了由ATP11c-CDC50A翻转维护的宿主酸素 (PS) 非对称性,用于病毒的进入和复制. 这种颠覆影响病毒病原和家禽健康.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 纽卡斯尔病病毒 (NDV) 是一种主要的鸟类病原体,造成重大经济损失.
- NDV感染与宿主脂质代谢有关,特别是酸 (PS) 非对称性.
- ATP11c-CDC50A复合体维持PS不对称性,这对细胞平衡至关重要,但可能被病毒利用.
研究的目的:
- 研究NDV在其生命周期中如何利用宿主PS和ATP11c-CDC50A复合体.
- 阐明NDV颠覆宿主脂质代谢以复制的机制.
主要方法:
- 在CRISPR-Cas9基因编辑中创建ATP11c淘汰细胞.
- 针对CDC50A的局部导向突变发生,以评估飞酶活性.
- 分析病毒复制,病毒释放和病毒样颗粒的产生.
主要成果:
- ATP11c淘汰赛损害了NDV复制和后代病毒的释放.
- CDC50A突变显著减少了PS的再分配,影响了flippase功能.
- 由NDV诱导的亡导致PS外部化,增强矩阵 (M) 蛋白质聚类和病毒样颗粒的产生.
结论:
- 新型冠状病毒利用ATP11c-CDC50A复合体来操纵PS不对称的病毒进入和复制.
- 病毒劫持了内叶PS以在血膜上固M蛋白质寡合化.
- 这些发现揭示了一种新的病毒病原机制,涉及对宿主脂质稳态的颠覆.
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