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Wenchun Fan¹, Katrina B Mar¹, Levent Sari²

¹Department of Microbiology, UT Southwestern Medical Center, Dallas, TX 75390, USA.

|June 1, 2021

概括

通过降解病毒蛋白2BC,E3无素连接酶TRIM7限制了肠道病毒. 病毒突变逃避TRIM7,导致小鼠的毒性增加和致命的胰腺炎.

科学领域:

病毒学
免疫学
分子生物学

背景情况:

脊椎动物利用干扰素反应和细胞内在的抗病毒蛋白来对抗病毒感染.
细胞内在免疫包括先前存在的抗病毒蛋白质,可提供即时的防御.
许多细胞内在抗病毒因子的精确机制尚不完全理解.

研究的目的:

识别和描述针对人类肠道病毒的细胞内在抗病毒效应剂.
阐明TRIM7限制肠道病毒复制的分子机制.
研究宿主限制因素对病毒适应的进化后果.

主要方法:

使用细胞培养模型研究TRIM7介导的肠道病毒限制.
采用生物化学测试来分析蛋白质无处不在和降解.
产生并表征具有特定点突变的病毒突变.
在小鼠模型中评估病毒复制和致病性.

主要成果:

鉴定了E3泛素连接酶TRIM7作为细胞内在的限制多个人类肠道病毒的因素.
证明TRIM7针对病毒的2BC蛋白进行无化和蛋白体降解.
显示TRIM7耐药的coxsackievirus在2C ATPase/helicase中发生突变,损害了细胞培养中的复制,但在小鼠中增加了毒性.
观察到抗病毒在小鼠中引起致命的胰腺炎.

结论:

通过降解病毒2BC蛋白质,TRIM7作为一种新型抗病毒效应剂来抑制肠道病毒.
病毒适应TRIM7涉及免疫逃避和复制能力之间的权衡.
像TRIM7这样的宿主限制因素可以驱动病毒进化,对病变产生重大影响.

关键词:

抗病毒免疫力 E3 无素结合酶进入病毒限制因素病毒的演变病毒病原性

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