伪狂犬病病毒VHS蛋白通过阻断NF-κB和IRF3核转位来取消干扰素反应
Zhenfang Yan1, Jiayu Yue1, Yaxin Zhang1
1Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China.
Virologica Sinica
|June 1, 2024
概括
伪病毒 (PRV) 使用其UL41蛋白来抑制宿主抗病毒防御,包括炎症性细胞因子产生和cGAS-STING信号传递. 这种免疫规避对于猪中PRV感染和病原发生至关重要.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 疹病毒,包括伪疹病毒 (PRV),采用各种策略来抵消宿主抗病毒机制,往往导致宿主细胞死亡.
- 猪病毒是一种著名的猪病原体,对严重的神经疾病和死亡率负责.
- 细胞亡是晚期PRV感染的一个特征.
研究的目的:
- 研究由UL41编码的病毒宿主关闭 (VHS) 蛋白在PRV与宿主抗病毒反应相互作用中的作用.
- 阐明UL41对抗宿主免疫力的分子机制,特别关注炎症性细胞因子产生和cGAS-STING通路.
主要方法:
- 研究UL41对PRV诱导的炎症性细胞因子激活的影响.
- 通过UL41评估了cGAS-STING介导的抗病毒活性的调节.
- 研究UL41对IRF3酸化和转位的影响.
- 在UL41 RNase域 (E192,D194,D195) 和UL41敲除实验中利用保存氨基酸的位点定向突变发生.
主要成果:
- 发现UL41可以抑制PRV诱导的炎症性细胞因子激活.
- UL41通过向IRF3来负面调节cGAS-STING介导的抗病毒活性,抑制其酸化和转位.
- 在UL41 RNase域或UL41敲击中的突变损害了PRV的免疫逃避能力.
结论:
- UL41蛋白质是PRV逃避宿主免疫反应战略的一个关键因素.
- UL41对IRF3的向对于抑制抗病毒活性和促进病毒感染至关重要.
- 了解UL41的功能,可以了解PRV的病原和潜在的治疗点.
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