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研究人类单细胞粘附,迁移和转移及其由寨卡病毒调节的情况

Emma Partiot¹, Diana Brychka¹, Raphael Gaudin¹

¹CNRS, Institut de Recherche en Infectiologie de Montpellier (IRIM), Montpellier 34293, France; Univ Montpellier, Montpellier 34090, France.

European journal of cell biology

|August 25, 2024

概括

寨卡病毒 (ZIKV) 通过颠覆活性细胞骨调节和LFA-1相互作用来增强单细胞粘附和转移到中枢神经系统. 了解这些病毒神经入侵机制为治疗提供了新的治疗点.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

人体单细胞是寨卡病毒 (ZIKV) 感染的关键目标.
单细胞迁移对于组织透至关重要,包括中枢神经系统 (CNS).
了解ZIKV对单细胞迁移的影响对于理解病毒神经入侵至关重要.

研究的目的:

研究ZIKV感染对人类单细胞粘附,迁移和转移的影响.
确定涉及ZIKV介导单细胞透的特定分子机制和途径.
探索抑制ZIKV诱导的神经侵入的潜在治疗点.

主要方法:

单细胞暴露于ZIKV,并监测它们的粘附性,迁移性和转移性.
使用了向actin聚合调节器 (例如mDia,Cdc42,Rac1,ROCK,Arp2/3,Myosin-II) 和LFA-1的药理抑制剂.
在人类大脑微血管内皮细胞 (hCMEC/D3) 上进行了转移试验.

主要成果:

ZIKV增强了单细胞对原的附着性,依赖于mDia和Cdc42.
通过原蛋白的单细胞迁移通常被actin调节剂抑制,ZIKV暴露的细胞表现出与对照细胞相似的特征.
单细胞在hCMEC/D3细胞中的转移取决于Rac1,ROCK和Cdc42.
抑制LFA-1 (BIRT377) 特别减少了ZIKV暴露的单细胞的转移,这表明在病毒神经入侵中具有附着后作用.

结论:

齐克病毒感染会改变单细胞的迁移性质,特别是增强粘附性并通过LFA-1促进转移.
这些发现揭示了促进病毒神经入侵的特定病毒与宿主相互作用.
准LFA-1是一种潜在的策略,可以抑制ZIKV感染细胞透到中枢神经系统.

关键词:

在Actin中的Actin是Actin.细胞骨架细胞骨架脑内皮质 (Endothelium) 是一个内皮.弗拉维病毒 (flavivirus) 是一种病毒.神经侵入是一种神经侵袭.在Rho GTPase中.

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