考克萨基病毒B3组调节ASS1介导的代谢重编程,并在病毒性心肌炎中促进巨细胞炎症两极分化
Qiong Liu1, Yinpan Shang1, Ziwei Tao1
1The First Affiliated Hospital of Nanchang University and School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang, China.
Journal of virology
|August 28, 2024
概括
考克萨基病毒B3 (CVB3) 感染引发病毒性心肌炎 (VMC) 通过上调ASS1,促进炎症. 素补充剂可以逆转这一过程,为VMC提供潜在的治疗方法.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
背景情况:
- 病毒性心肌炎 (VMC) 是一种严重的心脏病,通常是由Coxsackievirus B3 (CVB3) 引起的.
- 目前对VMC的治疗方法有限,这凸显了需要新的治疗策略.
- 在CVB3诱导的VMC中,早期的先天免疫反应,特别是巨细胞的作用,尚不清楚.
研究的目的:
- 阐明氨酸酸合成酶1 (ASS1) 在CVB3诱导的VMC病原体中的作用.
- 研究CVB3感染对尿素循环代谢和巨细胞两极分化的影响.
- 探索素补充剂对VMC的治疗潜力.
主要方法:
- 研究了CVB3,其蛋白VP2和ASS1降解之间的相互作用.
- 分析了CVB3对素消耗和尿素循环重编程的影响.
- 在CVB3感染和素补充剂的背景下评估了巨细胞两极分化和炎症反应.
主要成果:
- CVB3及其VP2蛋白抑制了ASS1.1的自降解.
- CVB3感染导致素缺乏,ASS1上调和尿素循环代谢重编程.
- 这种代谢转变激活了巨细胞,促进了促炎性两极分化,并加剧了VMC.
- 素补充剂抵消了这些影响,降低了ASS1的调节,使巨细胞极化正常化,并减少了VMC的严重程度.
结论:
- CVB3感染通过操纵ASS1代谢和巨细胞激活来促进VMC.
- ASS1被确定为VMC的新疗法标.
- 素补充剂证明了缓解CVB3诱导的VMC的治疗潜力.
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