感染SARS-CoV-2感染重新激活HIV-1复制从U1细胞中的潜伏状态
Xue Wang1, Weichun Tang2, Jiangqin Zhao1
1Division of Emerging and Transfusion Transmitted Diseases, Food and Drug Administration, Silver Spring, Maryland, USA.
Journal of cellular physiology
|May 11, 2025
概括
感染COVID-19可能会重新激活潜伏的HIV-1. 带有尖端蛋白删除 (RRAΔ) 的SARS-CoV-2变种增强了HIV-1复制和亡,可能有助于HIV-1生存.
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:
- COVID-19 (SARS-CoV-2) 影响全球数以百万计的人,包括艾滋病毒-1感染者.
- 感染SARS-CoV-2对HIV-1从潜伏期的重新激活的影响尚不清楚.
研究的目的:
- 调查SARS-CoV-2感染如何影响HIV-1从潜伏期的重新激活.
- 为了比较野生型的SARS-CoV-2和具有尖端蛋白RRA删除 (RRAΔ) 的变体对HIV-1复制的影响.
主要方法:
- 利用U1细胞系,作为潜伏HIV-1的一个模型.
- 采用实时PCR测定和西部斑分析来量化HIV-1RNA和蛋白质水平.
- 评估了宿主转录因子参与 (NFAT,NF-κB p65,Ap-1,Sp-1) 和亡途径.
主要成果:
- 感染SARS-CoV-2导致HIV-1RNA水平增加.
- 与野生型相比,SARS-CoV-2 RRAΔ变体显著增强了HIV-1复制.
- RRAΔ变异通过外部和内在途径诱导了更大的亡活性.
- 观察到NFAT,NF-κB p65,Ap-1,Sp-1,p-TEFb,Jak/Stat和TLR通路的参与.
结论:
- 感染SARS-CoV-2可能会重新激活潜伏的HIV-1复制.
- 在SARS-CoV-2尖端蛋白中的RRA删除可能调节HIV-1复制和亡,可能促进HIV-1生存.
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