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敏克肠炎病毒感染诱导细胞循环停止和自为其复制

Dong Lu-Jiao¹, Li Zhi-Juan², Sun Ying-Li¹

¹Shandong Provincial Key Laboratory of Zoonoses, Shandong Agricultural University, Taian, Shandong Province 271018, China; College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong Province 271018, China.

Veterinary microbiology

|January 11, 2025

概括

敏克肠炎病毒 (MEV) 通过其NS1蛋白质引起S相停止,影响病毒复制. 升级调节的TRIM23蛋白在MEV感染中也起作用.

科学领域:

病毒学病毒学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

鱼肠炎病毒 (MEV) 导致鱼的重大疾病.
MEV诱导的细胞循环停止的精确机制以及自在MEV复制中的参与尚未完全理解.

研究的目的:

研究MEV NS1蛋白在诱导细胞循环停止中的作用.
探索与自相关的蛋白TRIM23在MEV复制中的功能.

主要方法:

实验室CRFK细胞模型被用于研究MEV感染.
分析了MEV NS1蛋白域 (NLS和TAD) 对于它们在细胞循环停止中的作用.
蛋白质组概况确定了MEV感染期间TRIM23的上调.
进行了TRIM23的siRNA介导淘汰,以评估其对MEV复制的影响.

主要成果:

MEV感染和NS1蛋白诱导CRFK细胞中的S相停止.
NS1蛋白的NLS和TAD域对于诱导S相停止至关重要.
MEV感染导致了与自相关的蛋白TRIM23.3的显著上调.
TRIM23的淘汰影响了TBK1和p62蛋白水平,间接影响了MEV复制.

结论:

MEV感染诱导S相停止,部分由NS1蛋白的NLS和TAD域介导.
TRIM23的上调是对MEV感染的显著宿主反应,并影响病毒复制.
无论是S阶段停止还是TRIM23,都在子肠炎病毒的复制中起着至关重要的作用.

关键词:

自自是一种自的过程.细胞循环停止细胞循环停止鱼肠炎病毒的病毒蛋白质组学是指蛋白质组学.

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