CD147 facilitates HIV-1 infection by interacting with virus-associated cyclophilin A
CD147 facilitates HIV-1 infection by interacting with virus-associated cyclophilin A
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DOI：
10.1073/pnas.111583198
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发表时间：
2001-05-22
影响因子：
11.1
通讯作者：
Bukrinsky, M
中科院分区：
文献类型：
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作者：
Pushkarsky, T;Zybarth, G;Bukrinsky, M
亲环素A（CyPA）特异性地掺入HIV-1的病毒体中，并且已显示出显著增强细胞HIV-1感染的早期步骤。我们的初步研究表明，CD 147是细胞外CyPA的受体。在这里，我们证明了CyPA-CD 147相互作用在HIV-1感染的早期阶段的作用。人CD 147的表达在一个周期条件下增加了HIV-1的感染。然而，对缺乏CyPA的病毒（在环孢菌素A存在下产生的猿猴免疫缺陷病毒或HIV-1）感染的易感性不受CD 147的影响，病毒相关的CyPA与来自感染细胞的CD 147共免疫沉淀。抗CD 147抗体可抑制HIV-1进入，这可通过延迟HIV-1核心蛋白从细胞膜的易位和抑制病毒逆转录来证明。复制不需要CyPA的病毒（SIV或突变型HIV-1）对抗CD 147抗体的抑制作用具有抗性。这些结果表明，HIV-1进入依赖于病毒相关的CyPA和靶细胞上的CD 147之间的相互作用。
Cyclophilin A (CyPA) is specifically incorporated into the virions of HIV-1 and has been shown to enhance significantly an early step of cellular HIV-1 infection. Our preliminary studies implicated CD147 as a receptor for extracellular CyPA, Here, we demonstrate a role for CyPA-CD147 interaction during the early steps of HIV-1 infection. Expression of human CD147 increased infection by HIV-1 under one-cycle conditions. However, susceptibility to infection by viruses lacking CyPA (simian immunodeficiency virus or HIV-1 produced in the presence of cyclosporin A) was unaffected by CD147, Virus-associated CyPA coimmunoprecipitated with CD147 from infected cells. Antibody to CD147 inhibited HIV-1 entry as evidenced by the delay in translocation of the HIV-1 core proteins from the membrane and inhibition of viral reverse transcription. Viruses whose replication did not require CyPA (SIV or mutant HIV-1) were resistant to the inhibitory effect of anti-CD147 antibody. These results suggest that HIV-1 entry depends on an interaction between virus-associated CyPA and CD147 on a target cell.