Guntermann C, Murphy B J, Zheng R, Qureshi A, Eagles P A, Nye K E
Department of Immunology, St Bartholomew's and the Royal London School of Medicine and Dentistry, London, EC1A 7BE, United Kingdom.
Biochem Biophys Res Commun. 1999 Mar 16;256(2):429-35. doi: 10.1006/bbrc.1999.0333.
The human immunodeficiency virus-1 (HIV-1) utilises CD4 and certain beta-chemokine receptors, mainly CCR-5 and CXCR4, for attachment and virus entry into T-lymphocytes and monocytes/macrophages. CD4 and beta-chemokine receptors participate in intracellular signalling via protein tyrosine kinases and G-protein-coupled signalling. The factors which influence HIV-1 replication and the intracellular signalling mechanisms elicited by the virus are not well understood. In this study, it was demonstrated that exposure of peripheral blood lymphocytes (PBLs) to a T-cell tropic strain of HIV-1 evokes signal(s) which results in downregulation of intracellular cAMP. In addition, pre-incubation of PBLs with the Gi-protein inhibitor Pertussis toxin mediated a significant inhibition of HIV-1 replication. These data strongly suggest that HIV-1 employs CD4 receptors and Gi-coupled proteins for entry into target cells and that productive HIV-1 infection is dependent on an active signalling event.
人类免疫缺陷病毒1型（HIV-1）利用CD4和某些β趋化因子受体（主要是CCR-5和CXCR4）附着并进入T淋巴细胞和单核细胞/巨噬细胞。CD4和β趋化因子受体通过蛋白酪氨酸激酶和G蛋白偶联信号传导参与细胞内信号传导。影响HIV-1复制的因素以及该病毒引发的细胞内信号传导机制尚未完全清楚。在本研究中，已证明外周血淋巴细胞（PBL）暴露于T细胞嗜性的HIV-1毒株会引发导致细胞内cAMP下调的信号。此外，PBL与Gi蛋白抑制剂百日咳毒素预孵育可显著抑制HIV-1复制。这些数据强烈表明，HIV-1利用CD4受体和Gi偶联蛋白进入靶细胞，并且有效的HIV-1感染依赖于活跃的信号事件。
