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甲基胺诱导metallothionein 1表达和原发性人类艾滋病毒感染巨细胞的炎症现象
Jessica Weiselberg1, Meng Niu2, Cristian A Hernandez1
1Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA.
International journal of molecular sciences
|September 27, 2025
概括
艾滋病毒感染者 (PWH) 使用甲基胺会增加巨细胞中的核MT1蛋白,通过促进炎症反应,可能会恶化与艾滋病毒相关的神经认知障碍 (HIV-NCI).
科学领域:
- 神经免疫学 神经免疫学
- 病毒学 病毒学
- 毒理学 毒理学 毒理学
背景情况:
- 与艾滋病毒相关的神经认知障碍 (HIV-NCI) 影响高达50%的艾滋病毒感染者 (PWH).
- 中枢神经系统中感染艾滋病毒的巨细胞有助于神经元损伤.
- 甲基胺 (meth) 的使用加剧了PWH的认知衰退.
研究的目的:
- 调查是否使用甲基失调巨细胞的功能,有助于增加HIV-NCI.
- 为了描述暴露于甲基的HIV感染巨细胞的基因表达变化.
主要方法:
- 主要的人类巨细胞感染了艾滋病毒,并每天用甲基治疗五天.
- 用RNA测序来分析差异性基因表达.
- 评估了金属联蛋白1 (MT1) 的核定位和细胞因子/化学因子的产生.
主要成果:
- 甲基治疗增加了艾滋病毒感染巨细胞的核MT1局部化.
- 增加的核MT1与高的LPS诱导的CXCL8和CCL8.8相关.
- 增加TNF-α和IL-6的趋势被观察到以一种特定于捐赠者的方式.
结论:
- 艾滋病毒感染的巨细胞中重复暴露于甲基会增加核MT1.
- 这种机制可能会通过增强的炎症导致艾滋病毒-NCI的甲基中介性恶化.
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