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纽卡斯尔病病毒通过煽动氧化压力驱动的Sirtuin 7生产来调节其复制
1Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, Assam 781039, India.
The Journal of general virology
|February 20, 2024
概括
纽卡斯尔病病毒 (NDV) 感染通过调节sirtuin 7 (SIRT7) 蛋白水平,影响细胞氧化应激. 这种病毒策略通过改变NAD+代谢和宿主蛋白脱乙烯化来增强NDV复制.
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:
- 反应性氧物种 (ROS) 触发氧化压力,并激活细胞内的应激基因.
- 病毒可能利用宿主应激反应和蛋白质来促进其复制,但这些机制尚未完全理解.
研究的目的:
- 为了研究氧化应激反应如何影响纽卡斯尔病病毒 (NDV) 病变.
- 在氧化应激期间通过NDV感染调节的特定宿主基因的识别.
主要方法:
- 评估与细胞内ROS水平相关的NDV感染进展.
- 分析氧化应激反应基因的表达,重点关注素7 (SIRT7).
- 在DF-1细胞中调节SIRT7蛋白水平 (过度表达和淘汰),观察对NDV复制的影响.
主要成果:
- NDV感染的进展与细胞内ROS水平相关.
- NDV感染显著调节氧化应激反应基因*SIRT7*的表达.
- SIRT7调制 (过度表达/敲除) 影响NDV复制动态.
- SIRT7的激活与细胞蛋白脱乙的增加有关.
- 由NDV诱导的SIRT7改变了NAD+代谢 *in vitro*和 *in ovo*.
结论:
- NDV感染操纵宿主氧化应激反应,特别是调节SIRT7.
- 升高的NDV介导的SIRT7蛋白通过代谢NAD+进行宿主蛋白脱乙烯化来增强病毒复制.
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