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艾滋病毒-1 Vpr 抗击原始人类巨细胞中由PU.1驱动的抗病毒反应

Maria C Virgilio^1,2,3, Barkha Ramnani³, Thomas Chen^2,3,4

¹Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, MI, USA.

Nature communications

|July 1, 2024

概括

HIV-1 Vpr蛋白降解巨细胞中的PU.1转录因子,削弱抗病毒防御并增强HIV-1传播到T细胞. 这种机制在灵长类林氏病毒中保持着.

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:

艾滋病毒-1 Vpr 蛋白质通过降低宿主限制因素来促进病毒传播.
PU.1 是先天免疫基因表达的关键转录因子,包括那些针对HIV-1包裹 (Env) 的转录因子.

研究的目的:

阐明HIV-1 Vpr促进病毒传播的机制.
研究Vpr与与先天免疫有关的转录因子的相互作用.

主要方法:

转录组分析以确定针对Vpr的途径.
PU.1 在巨细胞中的沉默实验.
同免疫沉以研究蛋白质相互作用.
对Vpr对受感染和未受感染的旁观者细胞的影响的分析.

主要成果:

Vpr的目标是PU.1,这是对限制HIV-1 Env.原生免疫基因必不可少的转录因子.
在缺乏Vpr的细胞中抑制PU.1可以挽救Env的表达.
Vpr通过与DCAF1和Cul4A E3泛基因酶的相互作用诱导PU.1的蛋白质体降解.
在旁观者细胞中,Vpr抑制了先天免疫基因表达,而与病毒相关的Vpr可以降低PU.1.
Vpr的向PU.1的能力在灵长类林氏病毒中保持不变.

结论:

艾滋病毒-1 Vpr在巨细胞中对抗PU.1,抑制抗病毒免疫反应并促进病毒传播.
Vpr的机制涉及PU.1的直接降解,影响感染细胞和旁观者细胞.

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