病毒诱导的Abl和Fyn激酶信号允许coxsackievirus通过表皮紧密结口进入
Carolyn B Coyne1, Jeffrey M Bergelson
1Division of Infectious Diseases, The Children's Hospital of Philadelphia, University of Pennsylvania, PA 19104, USA.
组B的Coxsackievirus (CVB) 使用衰变加速因子 (DAF) 来触发信号通路. 这使得病毒能够移动到紧密的结点,并通过上皮屏障感染.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 组B的Coxsackievirus (CVBs) 必须突破上皮屏障以开始感染.
- 位于紧密的结点上的coxsackievirus和腺病毒受体 (CAR) 从顶端表面无法进入.
- CVBs经常与衰变加速因子 (DAF) 相互作用,这是一个GPI固的蛋白质.
研究的目的:
- 阐明CVBs穿越上皮质屏障的机制.
- 研究DAF和CAR在CVB感染中的作用.
- 为了确定CVB用于上皮细胞进入的信号通路.
主要方法:
- 使用细胞培养模型研究病毒与宿主相互作用.
- 利用激酶抑制剂和基因操纵来探测信号通路.
- 检查了病毒的进入和细胞内传输机制.
主要成果:
- 角DAF结合激活Abl酶,诱导Rac-依赖的活性蛋白重组,使病毒转移到紧密的结节.
- 在紧密的结点上,CAR相互作用会诱导囊体的结构变化,这对于病毒进入和RNA释放至关重要.
- DAF的参与也激活了Fyn激酶,导致洞穴酸化和洞穴介导的病毒吸收.
结论:
- CVBs利用DAF介导的信号来克服表皮屏障.
- 病毒劫持宿主细胞机械,涉及Abl和Fyn激酶,actin重塑和洞穴,以有效地进入.
- 了解这些机制,可以了解病毒病原和潜在的治疗点.
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