Chemokine coreceptor signaling in HIV-1 infection and pathogenesis.

Chemokine coreceptor signaling in HIV-1 infection and pathogenesis.
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DOI:
10.1371/journal.ppat.1000520
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发表时间:
2009-12
期刊:
影响因子:
6.7
通讯作者:
Yoder A
Yoder A
中科院分区:
医学1区
文献类型:
--
作者:
Wu Y;Yoder A

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HIV-1 包膜与其趋化因子辅助受体的结合介导两个主要的生物事件:膜融合和信号转导。融合过程已得到充分研究,但趋化因子辅助受体信号传导在病毒感染中的作用在过去十年中仍然难以捉摸。随着最近证明静息 CD4 T 细胞的 HIV 潜伏感染需要信号传导,需要彻底重新审视辅助受体信号传导问题。病毒介导的信号传导事件可能会促进体内各种免疫环境中的感染,这些环境中需要启动细胞条件;换句话说,HIV可能利用免疫细胞之间共享的趋化因子信号网络来获取下游细胞成分,从而可以作为打破细胞屏障的有效工具。这种病毒劫持的异常信号传导过程可能反过来促进发病机制。在这篇综述中,我们总结了过去和现在关于 HIV 辅助受体信号传导的研究。我们还讨论了辅助受体信号传导在促进病毒感染和发病机制中的可能作用。
Binding of the HIV-1 envelope to its chemokine coreceptors mediates two major biological events: membrane fusion and signaling transduction. The fusion process has been well studied, yet the role of chemokine coreceptor signaling in viral infection has remained elusive through the past decade. With the recent demonstration of the signaling requirement for HIV latent infection of resting CD4 T cells, the issue of coreceptor signaling needs to be thoroughly revisited. It is likely that virus-mediated signaling events may facilitate infection in various immunologic settings in vivo where cellular conditions need to be primed; in other words, HIV may exploit the chemokine signaling network shared among immune cells to gain access to downstream cellular components, which can then serve as effective tools to break cellular barriers. This virus-hijacked aberrant signaling process may in turn facilitate pathogenesis. In this review, we summarize past and present studies on HIV coreceptor signaling. We also discuss possible roles of coreceptor signaling in facilitating viral infection and pathogenesis.
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