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肠道病毒3C蛋白酶切割N4BP1以损害宿主炎症反应

Dongjie Zhang¹, Yifan Xie¹, Jie Cao¹

¹Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.

Journal of virology

|December 10, 2024

概括

肠病毒3C蛋白酶 (3Cpro) 切割N4BP1,这是NF-κB信号的调节器,损害了宿主免疫反应. 这项研究将N4BP1确定为一种新型基质,揭示了对病毒病原和宿主-病原体相互作用的见解.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

肠病毒3C蛋白酶 (3Cpro) 对于病毒复制和病变发生至关重要.
3Cpro针对宿主蛋白质,破坏抗病毒反应并促进感染.
了解3Cpro基质是破译病毒病原学的关键.

研究的目的:

为了识别和描述肠道病毒3Cpro.pro.的新基质.
研究N4BP1裂变在病毒病原和NF-κB信号传递中的作用.
探索3Cpro-N4BP1相互作用中的特定物种差异.

主要方法:

生物信息图案搜索使用FIMO识别潜在的3Cpro裂变地点.
生物化学分析证实N4BP1被各种肠道病毒3Cpros.
细胞生物学方法来评估N4BP1分裂对病毒感染期间NF-κB信号传递的影响.

主要成果:

鉴定出NEDD4结合蛋白1 (N4BP1) 是肠道病毒3Cpro.的新型基质.
人类N4BP1被多个人类肠道病毒3Cpros在Q816分裂,导致NF-κB调节功能的丧失.
鼠标N4BP1对人类肠道病毒3Cpro有耐药性,但对动物EMCV 3Cpro有敏感性,这表明该物种具有特定的裂纹.
内源N4BP1的裂变发生在病毒感染期间,不会影响病毒复制,但会损害宿主免疫信号.

结论:

N4BP1是肠道病毒3Cpro的新型基质,显著影响宿主NF-κB信号传递.
3Cpro对N4BP1的分裂是肠道病毒利用的保护机制,以抵消宿主防御.
3Cpro在N4BP1分裂中的特定物种差异突出了复杂的宿主-病原体相互作用,并为未来的研究提供了途径.

关键词:

3C蛋白酶是一种3C蛋白酶.N4BP1 一个问题.裂纹裂纹裂纹裂纹肠道病毒肠道病毒炎症反应是一种炎症反应.

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