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β趋化因子对嗜单核细胞性HIV-1感染的抑制作用。对结合后融合步骤的干扰。

Beta-chemokine inhibition of monocytotropic HIV-1 infection. Interference with a postbinding fusion step.

作者信息

Oravecz T, Pall M, Norcross M A

机构信息

Division of Hematologic Products, Bethesda, MD 20892, USA.

出版信息

J Immunol. 1996 Aug 15;157(4):1329-32.

PMID:8759710
Abstract

The beta-chemokines RANTES, MIP-1 alpha, and MIP-1 beta have potent suppressive effects on HIV-1 infection resulting from an early postbinding block in virus fusion and entry. Inhibition was observed only with monocytotropic isolates and mapped to the V3 region of the HIV-1 envelope. RANTES did not inhibit virus expression in chronically infected cells or reduce initial virus attachment to the cell membrane. Inhibitory activity required RANTES binding to the target cell but not G protein-mediated signaling or protein tyrosine kinase activity. The results are consistent with a reversible competitive mechanism of virus inhibition that prevents a V3-associated postbinding step in membrane fusion. The data support a role for a RANTES chemokine receptor as a coreceptor for monocytotropic-HIV-1.

摘要

β-趋化因子RANTES、MIP-1α和MIP-1β对HIV-1感染具有强大的抑制作用,这是由病毒融合和进入过程中结合后的早期阻断所致。仅在嗜单核细胞分离株中观察到抑制作用,且定位于HIV-1包膜的V3区域。RANTES不抑制慢性感染细胞中的病毒表达,也不减少病毒与细胞膜的初始附着。抑制活性需要RANTES与靶细胞结合,但不需要G蛋白介导的信号传导或蛋白酪氨酸激酶活性。这些结果与病毒抑制的可逆竞争机制一致,该机制可防止膜融合中与V3相关的结合后步骤。数据支持RANTES趋化因子受体作为嗜单核细胞-HIV-1共受体的作用。

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