一个UL26-PIAS1复合体在人类细胞巨乳病毒感染期间对抗抗病毒基因表达
Jessica Ciesla1, Kai-Lieh Huang1, Eric J Wagner1
1Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, New York, United States of America.
PLoS pathogens
|May 20, 2024
概括
人类细胞巨乳病毒 (HCMV) UL26蛋白质通过与PIAS1,一个SUMO结合酶相互作用来破坏先天免疫力. 这种相互作用阻止了STAT酸化和抗病毒基因表达,这对病毒传播至关重要.
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:
- 病毒逃避宿主天生的免疫力是感染的关键.
- 人类细胞巨乳病毒 (HCMV) UL26蛋白通过不清楚的机制抑制抗病毒基因表达.
研究的目的:
- 阐明HCMV UL26蛋白质对抗先天免疫信号的分子机制.
主要方法:
- 利用TurboID驱动的近距离蛋白学来识别UL26在HCMV感染期间相互作用的蛋白质.
- 研究UL26蛋白相互作用对STAT信号和抗病毒反应的功能影响.
主要成果:
- HCMV UL26蛋白与STAT家族成员和PIAS (激活STAT的蛋白抑制剂) 蛋白形成复合体,包括PIAS1.
- UL26抑制STAT酸化,并对抗干扰素-α (IFNα) 和瘤缩因子-α (TNFα) 诱导的转录激活.
- PIAS1无活化模仿UL26缺乏HCMV感染的抗病毒状态,对于HCMV细胞间传播至关重要.
结论:
- UL26-PIAS1相互作用对于HCMV调节内在抗病毒防御是至关重要的.
- HCMV UL26利用PIAS1抑制宿主抗病毒反应,促进病毒感染和传播.
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