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在接受ART治疗的SIV感染中,单细胞/巨细胞的持续激活和细胞衰老

Yilin Chen^1,2, Xiaofeng Ding^1,2, Sonalika Ray³

¹Tulane National Biomedical Research Center, Covington, LA 70433, USA.

bioRxiv : the preprint server for biology

|November 24, 2025

概括

抗逆转录病毒疗法 (ART) 抑制HIV,但慢性感染会导致持续的炎症和与衰老相关的问题. 准炎症酶,NF-κB和衰老可能有助于减少艾滋病毒感染者的非艾滋病并发症.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
基因组学就是基因组学.

背景情况:

接受抗逆转录病毒治疗 (ART) 的艾滋病毒感染者 (PLWH) 仍然面临慢性炎症,免疫功能障碍和并发症.
了解持续炎症背后的机制,尽管病毒抑制对于改善长期健康结果至关重要.

研究的目的:

在猿类免疫缺陷病毒 (SIV) 感染和ART治疗期间,研究外周血液单核细胞 (PBMC) 的纵向转录变化.
在长期ART下识别导致慢性SIV感染持续性炎症和并发症的分子途径.

主要方法:

使用SIV感染的 rhesus macaque PBMCs的散装RNA测序进行长度转录组分析,分为四个阶段:感染前,急性感染,短期ART和长期ART.
脏组织的蛋白质分析和动脉的病理评估,以确认分子发现并评估血管变化.

主要成果:

急性SIV感染引发了抗病毒和炎症反应,这些反应被短期ART逆转.
长期的ART抑制了病毒病,但重新激活了先天性免疫通路,包括TLR,NF-κB和炎症体信号,以及巨细胞激活和衰老.
血管分析揭示了富含巨细胞的斑块与衰老细胞和血栓形成,模仿艾滋病毒相关的动脉生成.

结论:

ART有效地解决了急性感染引起的免疫失调,但慢性SIV感染维持了与血管损伤和衰老相关的炎症状态.
持续性炎症是由巨细胞和TLR激活驱动的,独立于病毒载量.
准炎症体,NF-κB和衰老途径是缓解PLWH非艾滋病并发症的潜在策略.

关键词:

艺术艺术艺术艺术在IL-27和IL-27之间.在 NFκBB 的情况下.在RNA-seqqq.这就是SIV SIV.动脉样硬化动脉样硬化卡斯帕斯-1酶是一种炎症导致的炎症.巨细胞是一个巨细胞.

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