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β趋化因子受体CCR3和CCR5促进原发性HIV-1分离株的感染。

The beta-chemokine receptors CCR3 and CCR5 facilitate infection by primary HIV-1 isolates.

作者信息

Choe H, Farzan M, Sun Y, Sullivan N, Rollins B, Ponath P D, Wu L, Mackay C R, LaRosa G, Newman W, Gerard N, Gerard C, Sodroski J

机构信息

Division of Human Retrovirology Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

出版信息

Cell. 1996 Jun 28;85(7):1135-48. doi: 10.1016/s0092-8674(00)81313-6.

Abstract

We examined the ability of chemokine receptors and related G protein-coupled receptors to facilitate infection by primary, clinical HIV-1 isolates. CCR5, when expressed along with CD4, the HIV-1 receptor, allowed cell lines resistant to most primary HIV-1 isolates to be infected. CCR3 facilitated infection by a more restricted subset of primary viruses, and binding of the CCR3 ligand, eotaxin, inhibited infection by these isolates. Utilization of CCR3 and CCR5 on the target cell depended upon the sequence of the third variable (V3) region of the HIV-1 gp120 exterior envelope glycoprotein. The ability of various members of the chemokine receptor family to support the early stages of HIV-1 infection helps to explain viral tropism and beta-chemokine inhibition of primary HIV-1 isolates.

摘要

我们研究了趋化因子受体及相关G蛋白偶联受体促进原发性临床HIV-1分离株感染的能力。当CCR5与HIV-1受体CD4共同表达时,可使对大多数原发性HIV-1分离株具有抗性的细胞系被感染。CCR3促进了更具局限性的原发性病毒亚群的感染,且CCR3配体嗜酸性粒细胞趋化因子的结合可抑制这些分离株的感染。靶细胞上CCR3和CCR5的利用取决于HIV-1 gp120外膜糖蛋白第三个可变(V3)区的序列。趋化因子受体家族的各个成员支持HIV-1感染早期阶段的能力有助于解释原发性HIV-1分离株的病毒嗜性和β趋化因子抑制作用。

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