EV71 5'UTR与3D蛋白相互作用,通过AKT-mTOR途径影响复制
Xiaoying Xu1, Shao Ma2, Ziwei Liu3
1School of Public Health, Cheeloo College of Medicine, Shandong University, No. 44 Wenhua West Road, Lixia District, Jinan, 250012, China.
Virology journal
|May 22, 2024
概括
这项研究揭示了Enterovirus 71 (EV71) 5'UTR与3D蛋白相互作用,以调节病毒复制. 在EV71中发生的特定突变
科学领域:
- 病毒学 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:
- 肠道病毒71 (EV71) 是导致手足口病 (HFMD) 的重要原因,通常导致严重的神经并发症.
- 以前的研究表明,EV71 5'未翻译区域 (5'UTR) 与3D蛋白之间的潜在相互作用,但其在病毒复制中的作用仍然不清楚.
研究的目的:
- 为了研究EV71 5'UTR和3D蛋白之间的相互作用.
- 确定这种相互作用对病毒复制和宿主细胞自的影响.
主要方法:
- 在毒性EV71菌株中的4个5'UTR位点和2个3D蛋白位点的突变发生.
- 分析突变病毒复制及其对细胞自的影响.
- 评估自途径,包括自细胞积累,自细胞降解和AKT/mTOR信号传递.
主要成果:
- 单个5'UTR突变,除了一个外,与毒性原始菌株相比,减弱了病毒复制.
- 同突变菌株表现出各种复制特征,其中5种显示出相互作用的证据.
- 高复制性菌株促进了自细胞积累,阻碍了自细胞分解,并抑制了AKT/mTOR酸化.
- 低复制性菌株显示宿主细胞自的最小调节.
结论:
- EV71 5'UTR与3D蛋白相互作用,影响病毒复制.
- 特定的共同突变 (S37N-nt88C/T,S37N-nt574T/A,R142K-nt574T/A) 通过抑制AKT-mTOR自途径来促进病毒复制.
- 其他共同突变 (R142K-nt88C/T,R142K-nt157G/A) 通过减少AKT-mTOR通路的抑制来减少病毒复制.
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