Statin compounds reduce human immunodeficiency virus type 1 replication by preventing the interaction between virion-associated host intercellular adhesion molecule 1 and its natural cell surface ligand LFA-1
Statin compounds reduce human immunodeficiency virus type 1 replication by preventing the interaction between virion-associated host intercellular adhesion molecule 1 and its natural cell surface ligand LFA-1
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DOI：
10.1128/jvi.78.21.12062-12065.2004
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发表时间：
2004-11-01
影响因子：
5.4
通讯作者：
Tremblay, MJ
中科院分区：
文献类型：
--
作者：
Giguère, JF;Tremblay, MJ
多种宿主因子，包括 I 型人类免疫缺陷病毒 (HIV-1) 获得的膜蛋白，在 HIV-1 吸附到宿主细胞上的过程中发挥着主导作用。例如，整合素细胞间粘附分子 1 (ICAM-1)，一旦被 HIV-1 获得，就会通过与 LFA-1 连接来促进病毒感染。我们测试了他汀类药物减少 HIV-1 复制的能力，基于这些化合物已被证明可以阻断 ICAM-1-LFA-1 相互作用的想法。我们的数据表明，他汀类药物通过抑制 ICAM-1-LFA-1 相互作用来减少 HIV-1 对靶细胞的附着。他汀类药物限制病毒复制初始步骤的能力可能是治疗 HIV-1 感染的一种有趣的方法。
A variety of host factors, including membrane proteins acquired by human immunodeficiency virus type I (HIV-1), play a dominant role in HIV-1 adsorption onto host cells. Examples include the integrin intercellular adhesion molecule 1 (ICAM-1), which, once acquired by HIV-1, promotes virus infectivity via ligation to LFA-1. We tested the ability of statins to diminish HIV-1 replication, based on the idea that these compounds have been shown to block ICAM-1-LFA-1 interactions. Our data indicate that statins diminish HIV-1 attachment to target cells by suppressing ICAM-1-LFA-1 interactions. The capacity of statins to limit the initial steps in virus replication could represent an interesting approach for the treatment of HIV-1 infection.