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全基因组的CRISPR屏幕识别了ALG5,ALG6,NF2和FUT8作为参与传染性胃肠炎病毒感染的关键宿主蛋白

Zhihua Feng¹, Xinyan He², Minhua Lin²

¹Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, Fujian Normal University, Qishan Campus, Fuzhou, Fujian, 350117, China; College of Life Science, Fujian Normal University Qishan Campus, Fuzhou, Fujian, 350117, China; Key Laboratory of OptoElectronic Science and Technology for Medicine of Ministry of Education, Fujian Normal University, Fuzhou, Fujian, 350117, China; College of Photonic and Electronic Engineering, Fujian Normal University, Fuzhou, Fujian, 350117, China; Fuzhou Hospital of Traditional Chinese Medicine Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350001, China.

International journal of biological macromolecules

|November 8, 2025

概括

研究人员确定了关键宿主因素,包括ALG5,ALG6,NF2和FUT8,对于猪中传染性胃肠炎病毒 (TGEV) 感染至关重要. 这一发现为开发针对TGEV的抗病毒策略提供了新的目标.

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:

传染性胃肠炎病毒 (TGEV) 对全球猪生产构成重大威胁.
目前对TGEV的控制策略主要依赖于接种疫苗,因为缺乏有效的抗病毒疗法.

研究的目的:

通过全基因组CRISPR/Cas9选,识别TGEV感染所必需的宿主因素.
阐明通过确定宿主因素支持TGEV复制的独特机制.

主要方法:

在猪IPEC-J2细胞中进行全基因组CRISPR/Cas9查.
宿主因子的功能性特征,包括基因淘汰和酶抑制.
分析病毒吸附,内化和复制过程.
对宿主-病原体蛋白相互作用的研究.

主要成果:

确定了与黄素相关的糖化5 (ALG5),与黄素相关的糖化6 (ALG6) 和神经纤维素2 (NF2) 对于TGEV感染至关重要,它们通过pAPN转录或N-糖化影响病毒吸附和内化.
图尼卡米辛治疗抑制N-糖化抑制了TGEV感染.
基转移酶8 (FUT8) 淘汰特异性损害了病毒内部化和早期复制,通过影响双膜囊泡 (DMV) 形成,独立于其酶活性.
发现FUT8与TGEV非结构蛋白NSP3和NSP4相互作用,以促进DMV生物发生.

结论:

独特的宿主因素,ALG5,ALG6,NF2和FUT8,在TGEV生命周期的不同阶段起着至关重要的作用.
FUT8与病毒蛋白的相互作用对DMV形成至关重要,这是TGEV复制的关键步骤.
这些发现为TGEV病原体提供了新的见解,并确定了抗病毒干预的潜在目标.

关键词:

这是一个CRISPR屏幕.在TGEVV中,我们可以看到.主体因子是宿主因子.感染的感染感染.

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