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PRRSV劫持了DDX3X蛋白,并诱导铁灭,以促进病毒复制

Qian Mao¹, Shengming Ma², Shuangyu Li¹

¹College of Veterinary Medicine, Northwest Agriculture and Forestry University, Yangling, China.

Veterinary research

|August 18, 2024

概括

猪生殖和呼吸系统综合征病毒 (PRRSV) 感染会增加DEAD-box酶3 (DDX3X) 的表达,促进病毒复制和铁亡. 抑制DDX3X会减少PRRSV后代,揭示了一个关键的宿主-病原体相互作用.

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:

猪生殖和呼吸系统综合征病毒 (PRRSV) 在猪业中造成重大经济损失.
死亡盒螺旋酶3 (DDX3X) 参与RNA代谢,免疫反应和病毒感染.
在PRRSV感染中DDX3X的作用在很大程度上是未知的.

研究的目的:

调查DDX3X在PRRSV复制中的作用.
阐明DDX3X影响PRRSV感染的潜在机制.
探索DDX3X,铁和PRRSV扩散之间的关系.

主要方法:

马克-145细胞的PRRSV感染.
使用RK-33抑制剂和siRNAs操纵DDX3X表达.
过度表达的DDX3X.
转录学和代谢学分析.
传输电子显微镜 (TEM). 传输电子显微镜.

主要成果:

在宿主细胞中,PRRSV感染显著上调DDX3X表达.
减少DDX3X表达抑制了PRRSV后代的产生,而过度表达则增强了它.
DDX3X沉默影响了铁亡,FoxO信号传递和谷甲代谢.
感染PRRSV的细胞表现出铁灭的特征,而这些特征在DDX3X受抑制的细胞中是不存在的.
药物诱导的铁亡促进了PRRSV的复制,这表明了复杂的相互作用.

结论:

在促进PRRSV复制方面,DDX3X起着至关重要的作用.
通过DDX3X介导的机制,PRRSV感染可能会诱导铁亡,以增强病毒扩散.
准DDX3X或了解其与铁亡途径的相互作用可能为PRRSV控制提供新的策略.

关键词:

这是一个DDX3XX.PRRSVV 在这个问题上.铁性化 (ferroptosis) 是一种代谢组代谢组的代谢转录组 (transcriptome) 是一个转录组.

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