CC CKR5:一个RANTES,MIP-1alpha,MIP-1beta受体作为巨热性HIV-1的融合辅因子
G Alkhatib1, C Combadiere, C C Broder
1Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
Science (New York, N.Y.)
|June 28, 1996
概括
人类免疫缺陷病毒1型 (HIV-1) 进入CD4+细胞需要融合辅因子. CC CKR5作为宏热性HIV-1菌株的融合辅因子,调解病毒的进入.
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:
- 人类免疫缺陷病毒1型 (HIV-1) 进入目标细胞需要在CD4+细胞表面表达的特定融合辅因子.
- 素是一种G蛋白结合受体,作为T细胞系热带HIV-1分离体的辅因子.
- 众所周知,像RANTES,MIP-1alpha和MIP-1beta这样的化学因子可以抑制巨热性HIV-1分离体的感染.
研究的目的:
- 研究CC CKR5作为巨热性HIV-1菌株潜在的融合辅因子的作用.
- 为了确定CC CKR5是否在对巨热性HIV-1包膜糖蛋白 (Envs) 的反应中调解细胞融合.
主要方法:
- 评估化基因 (RANTES,MIP-1alpha,MIP-1beta) 对由特定的HIV-1 Envs介导的细胞融合的抑制作用.
- 在CD4表达的非人类细胞中表达重组CC CKR5,以评估它们与不同HIV-1 Envs的融合能力.
- 在各种细胞类型中检测CC CKR5信使RNA (mRNA),以将其存在与对巨热性HIV-1分离物的敏感性相关联.
主要成果:
- 化学物质RANTES,MIP-1alpha和MIP-1beta选择性地抑制了由巨热性HIV-1分离物的信封糖蛋白介导的细胞融合.
- 再组合CC CKR5表达染了CD4表达的非人类细胞易于融合,特别是与巨热带Envs.
- 主要检测到CC CKR5 mRNA是在已知易受巨热性HIV-1感染的细胞类型中.
结论:
- CC CKR5作为HIV-1的巨热带菌株的一个关键的融合辅因子.
- 这些发现确定CC CKR5是某些HIV-1分离体细胞热带的关键决定因素.
- 了解这些辅助因子相互作用对于开发针对HIV-1的向抗病毒疗法至关重要.
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