艾滋病毒感染不需要其受体CD4的内细胞分裂
P J Maddon1, J S McDougal, P R Clapham
1Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
Cell
|September 9, 1988
概括
人类免疫缺陷病毒 (HIV) 通过直接融合进入细胞,而不是内细胞分裂,尽管CD4分子可以被内化. 这项研究研究了使用CD4突变体的HIV进入机制.
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:
- CD4分子对T细胞功能至关重要,并作为人类免疫缺陷病毒 (HIV) 的受体.
- CD4+ T细胞可以通过醇或抗原呈现细胞的刺激将CD4分子内部化.
- 艾滋病毒进入细胞的机制,无论是通过内细胞结合还是直接融合,仍然是研究的一个领域.
研究的目的:
- 阐明艾滋病毒进入CD4+T细胞的机制.
- 为了确定艾滋病毒是否通过受体介导的内细胞分裂或直接与细胞膜的病毒融合而进入.
- 为了研究CD4分子内细胞分裂在HIV感染中的作用.
主要方法:
- 构建两个CD4蛋白突变体,细胞质域内细胞分裂受损.
- 使用表达野生型或突变CD4的HeLa细胞系进行定量感染性研究.
- 评估HIV结合和随后的CD4内细胞化.
主要成果:
- 表达野生型或突变CD4的HeLa细胞系对艾滋病毒感染的敏感性相等.
- 艾滋病毒与CD4+T细胞结合并没有导致CD4内细胞分裂.
- 突变的CD4分子,在内细胞分裂中受损,并没有改变HIV感染性.
结论:
- 艾滋病毒进入细胞是通过病毒包裹与细胞膜的直接融合而发生的.
- CD4分子内部化不是艾滋病毒进入的先决条件.
- CD4分子与艾滋病毒的相互作用不需要受体介导的内细胞分裂来进入病毒.
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