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长非编码RNA转移相关的肺腺癌转录1 通过调节巨细胞中的微RNA促进HIV-1复制
Zhihong Yuan1,2, Yunlong Huang3, Ruxana T Sadikot1,2
1VA Nebraska Western Iowa Health Care System, Omaha, Nebraska, USA.
Journal of virology
|May 31, 2023
概括
人类免疫缺陷病毒-1 (HIV-1) 感染诱导巨细胞中的长非编码RNA MALAT1,通过调节miR-150/SOCS1通路促进病毒复制. 针对MALAT1提供了一种潜在的治疗策略,以消除HIV-1储存库.
科学领域:
- 分子生物学分子生物学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 巨细胞作为人类免疫缺陷病毒-1 (HIV-1) 的持久储存库,即使在抗逆转录病毒治疗中也阻碍了根除.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是HIV-1/AIDS病原体的调节者,但它们在病毒复制中的特定作用和机制在很大程度上仍未被探索.
- 了解lncRNA的参与对于开发针对免疫细胞内潜伏的HIV-1储存器的策略至关重要.
研究的目的:
- 研究lncRNA转移相关的肺腺癌转录1 (MALAT1) 在调节巨细胞内的HIV-1复制中的作用.
- 阐明MALAT1,微RNA和炎症基因相互作用以影响HIV-1复制的分子机制.
- 探索针对MALAT1作为针对HIV-1储存体的治疗策略的潜力.
主要方法:
- 对HIV-1感染巨细胞中基因表达调节的分析.
- RNA免疫沉 (RIP) 测试用于验证分子相互作用.
- 使用SN50 (NF-κB p50抑制剂) 和MALAT1反感性寡核酸 (ASO) 的抑制研究.
主要成果:
- 艾滋病毒-1感染上调了MALAT1,这反过来又调节了miR-155和miR-150-5p的表达.
- 马拉特1通过通过海绵化miR-150-5p增加细胞因子信号传导1 (SOCS1) 表达的抑制剂来促进HIV-1复制,激活TREM 1/CIRP通路.
- 使用ASO抑制MALAT1显著降低了HIV-1p24的产生,HIV-1Gag的表达和促炎性细胞因子的释放.
结论:
- 艾滋病毒-1感染诱导巨细胞中的MALAT1,导致miR-150-5p减少和SOCS1增加,从而促进病毒复制和重新激活.
- MALAT1/miR-150-5p/SOCS1轴是HIV-1感染中巨细胞微环境的关键调节者.
- 向MALAT1为消除免疫细胞中的HIV-1储存体提供了一个有希望的治疗途径.
关键词:
艾滋病病毒-1 艾滋病病毒-1马拉特语 马拉特语 马拉特语在SOCS1中,SOCS1是SOCS1的组成部分.在TREM-1中,巨细胞是什么?巨细胞是什么?在 miR-150-5p 中使用.在 miR-155 系统中,它是 miR-155 的.更多相关视频
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