A dual-tropic primary HIV-1 isolate that uses fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors
A dual-tropic primary HIV-1 isolate that uses fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors
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DOI：
10.1016/s0092-8674(00)81314-8
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发表时间：
1996-06-28
期刊：
影响因子：
64.5
通讯作者：
Doms, RW
中科院分区：
文献类型：
--
作者：
Doranz, BJ;Rucker, J;Doms, RW
在这里，我们展示了β-趋化因子受体CKR-5作为M嗜性HIV病毒的辅助因子。表达CKR-5和CD4使不允许的细胞与表达M嗜性而不是T嗜性的HIV-1包膜蛋白的细胞形成合胞体。CKR-5和CD4的表达可以使M嗜性病毒株进入，但不能进入T嗜性病毒株。双嗜性原代HIV-1分离株(89.6)同时利用Fusin和CKR-5作为进入辅因子。表达89.6 env蛋白的细胞与表达CD4和Fusin或CKR-5的QT6细胞形成合胞体。β-趋化因子受体CKR-3和CKR-2b支持HIV-1 89.6 env介导的合胞体形成，但不支持任何T嗜性或M嗜性毒株的融合。我们的结果提示，疾病进展的T嗜性病毒可能是从病毒感染早期流行的纯M嗜性病毒进化而来，通过使病毒能够使用多个进入辅助因子的env蛋白的变化。
Here, we show that the beta-chemokine receptor CKR-5 serves as a cofactor for M-tropic HIV viruses. Expression of CKR-5 with CD4 enables nonpermissive cells to form syncytia with cells expressing M-tropic, but not T-tropic, HIV-1 env proteins. Expression of CKR-5 and CD4 enables entry of a M-tropic, but not a T-tropic, virus strain. A dual-tropic primary HIV-1 isolate (89.6) utilizes both Fusin and CKR-5 as entry cofactors. Cells expressing the 89.6 env protein form syncytia with QT6 cells expressing CD4 and either Fusin or CKR-5. The beta-chemokine receptors CKR-3 and CKR-2b support HIV-1 89.6 env-mediated syncytia formation but do not support fusion by any of the T-tropic or M-tropic strains tested. Our results suggest that the T-tropic viruses characteristic of disease progression may evolve from purely M-tropic viruses prevalent early in virus infection through changes in the env protein that enable the virus to use multiple entry cofactors.