艾滋病毒-1病毒进入CD4+细胞的过程中,通过化学因子受体CC-CKR-5进行介导
T Dragic1, V Litwin, G P Allaway
1The Aaron Diamond AIDS Research Center, The Rockefeller University, New York 10016, USA.
Nature
|June 20, 1996
概括
像MIP-1alpha,MIP-1beta和RANTES这样的β-化学因子可以抑制HIV-1进入CD4+T细胞. 受体CC-化学因子受体5 (CC-CKR-5) 被确定为NSIHIV-1感染的关键因素.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 已知β-化学因子 (MIP-1alpha,MIP-1beta,RANTES) 抑制某些类型1的人类免疫缺陷病毒 (HIV-1) 菌株的感染.
- 来自一些暴露于HIV-1的未感染个体的CD4+ T细胞对NSIHIV-1感染具有抵抗力,并产生升高的β-化学因子.
研究的目的:
- 调查β-化学因子抑制HIV-1感染的机制.
- 为了确定参与NSIHIV-1进入和融合的细胞受体.
主要方法:
- 用于测量β-化学因子对HIV-1的抑制.
- 细胞融合试验用于评估环境介导的膜融合.
- 在CD4+细胞中的β-化学因子受体的表达分析.
主要成果:
- 在入门阶段,MIP-1alpha,MIP-1beta和RANTES抑制NSIHIV-1感染.
- 这些化学因子还阻断了环境介导的细胞-细胞膜融合.
- 在CD4+细胞中CC-化学因子受体5 (CC-CKR-5) 的表达赋予了对NSIHIV-1感染和环境介导融合的敏感性.
- CC-CKR-5被确定为NSI初级HIV-1菌株的第二受体.
结论:
- 在限制NSIHIV-1感染方面,β-化学基因起着至关重要的作用.
- CC-CKR-5是一种关键的细胞受体,介导NSIHIV-1的进入和融合,作为病毒的共同受体.
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