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通过HIV-1 Tat-TRAF6交叉对话增强NF-κB激活

Yang Li¹, Xi Liu², Koh Fujinaga³

¹Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA.

Science advances

|January 19, 2024

概括

艾滋病毒-1 Tat 蛋白通过直接与 TRAF6.6 相互作用,激活核因子 κB (NF-κB) 信号. 这种相互作用增强了病毒转录,并在HIV和SIV菌株中保持.

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:

塔特蛋白对HIV-1和SIV转录至关重要.
已知Tat在激活核因子kB (NF-kB) 信号传递中的作用,但其机制尚不清楚.

研究的目的:

阐明HIV-1 Tat蛋白激活NF-κB信号传递的分子机制.
研究Tat和TRAF6在调节病毒转录中的相互作用.

主要方法:

测试Tat和TRAF6.6之间的直接相互作用.
对TRAF6的寡合化和无处不在的分析.
评估NF-κB通路激活和病毒转录.
功能性测试涉及TRAF6过度表达和敲击.

主要成果:

塔特直接与TRAF6相互作用,这是正规NF-κB通路的上游调节器.
这种相互作用促进了TRAF6的寡合化,自化和K63连接的多化链合成.
Tat-TRAF6相互作用增强NF-κB通路激活,导致HIV-1转录的增加.
过度表达TRAF6会激活HIV-1的转录,而TRAF6的倒置会抑制它.
通过TRAF6对NF-κB的Tat介导激活在HIV-1,HIV-2和SIV中保持.

结论:

艾滋病毒-1 Tat蛋白通过与TRAF6.6的相互作用直接激活NF-κB信号传递.
这种机制增强了病毒转录,并在不同的lentiviruses中保存.
这项研究揭示了一种新的途径,HIV-1可以操纵宿主细胞机械进行复制.

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