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全基因组的CRISPR/Cas9屏幕显示了HIV共受体CXCR4的JunB下调

William J Schulze¹, Devon A Gregory¹, Marc C Johnson¹

¹Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, United States.

Frontiers in microbiology

|June 5, 2024

概括

研究人员确定JunB是人类免疫缺陷病毒1型 (HIV-1) 复制所必需的关键宿主因子. 敲除JunB通过降低CXCR4的调节来阻止HIV-1感染,CXCR4是病毒进入的关键共受体.

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:

人类免疫缺陷病毒1型 (HIV-1) 的复制取决于宿主细胞因素.
之前对宿主因子的选已经产生了有限的可重复结果.
为了全面了解HIV-1感染,还需要确定新的宿主病毒相互作用.

研究的目的:

通过全基因组选,识别HIV-1感染所必需的新型宿主因素.
描述在病毒复制周期中确定宿主因素的作用.

主要方法:

在使用HIV诱导的细胞死亡进行选择的TZM-GFP记者细胞中进行全基因组CRISPR/Cas9选.
感染HIV-1_NL4-3并通过高通量测序对幸存细胞进行分析.
产生JunB淘汰 (KO) 细胞系和评估HIV-1感染水平.
在JunB KO细胞中进行CXCR4再引入实验,以验证发现.

主要成果:

转录因子JunB被确定为HIV-1感染所需的关键宿主因子.
JunB淘汰赛细胞对HIV-1_NL4-3感染表现出抵抗力.
在JunBKO细胞中,HIV-1感染阻断被归因于CXCR4表达的下调.
重新引入CXCR4恢复了JunBKO细胞中的HIV-1感染水平.

结论:

JunB在TZM-GFP细胞中调节CXCR4表达方面发挥着至关重要的作用.
通过JunB调节CXCR4的下调显著影响CXCR4热性HIV-1感染.
针对JunB-CXCR4轴提出了针对HIV-1的治疗干预的潜在策略.

关键词:

这就是CRISPR/Cas9的作用.CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4C 艾滋病病毒艾滋病病毒艾滋病病毒 JunB JunB JunB JunB JunB JunB JunB JunB JunB JunB JunB JunB JunB 主体因素是宿主因素.

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