Human immunodeficiency virus (HIV) binds to cells via an interaction between CD4 and the virus envelope glycoprotein, gp120. Previous studies have localized the high affinity binding site for gp120 to the first domain of CD4, and monoclonal antibodies (mAbs) reactive with this region compete with gp120 binding and thereby block virus infectivity and syncytium formation. Despite a detailed understanding of the binding of gp120 to CD4, little is known of subsequent events leading to membrane fusion and virus entry. We describe two new mAbs reactive with the third domain of CD4 that inhibit steps subsequent to virus binding critical for HIV infectivity and cell fusion. Binding of recombinant gp120 or virus to CD4 is not inhibited by these antibodies, whereas infection and syncytium formation by a number of HIV isolates are blocked. These findings demonstrate that in addition to virus binding, CD4 may have an active role in membrane fusion.

译文

人类免疫缺陷病毒(HIV)通过CD4和病毒包膜糖蛋白gp120之间的相互作用与细胞结合。先前的研究已经将gp120的高亲和力结合位点定位在CD4的第一个域,并且与该区域反应的单克隆抗体(mAb)与gp120结合竞争,从而阻断了病毒的感染性和合胞体的形成。尽管对gp120与CD4的结合有详细的了解,但对导致膜融合和病毒进入的后续事件知之甚少。我们描述了与CD4的第三个域具有反应性的两个新的单克隆抗体,可抑制继病毒结合后对HIV感染性和细胞融合至关重要的步骤。重组gp120或病毒与CD4的结合不受这些抗体的抑制,而许多HIV分离株的感染和合胞体形成却被阻止。这些发现表明,除病毒结合外,CD4可能在膜融合中发挥积极作用。

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