Department of Microbiology and Immunology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York 14214, United States.
Biochemistry. 2011 Aug 16;50(32):6966-72. doi: 10.1021/bi201014b. Epub 2011 Jul 15.
HIV entry occurs by concerted conformational changes in the envelope protein complex on the surface of the virus. This complex is made up of a trimer of heterodimers of two subunits: surface subunit, gp120, and transmembrane subunit, gp41. Conformational changes in the envelope complex allow gp41 to mediate membrane fusion leading to exposure of two gp41 regions: N-heptad repeat (NHR) and C-heptad repeat (CHR). Peptides from the NHR or the CHR have been found to inhibit HIV entry. Herein we show that we can covalently inhibit HIV viral entry by permanently trapping the gp41 intermediate on the virus surface using a covalently reactive group on inhibitory peptides. This is evidence showing that vulnerable conformational intermediates exist transiently during HIV viral entry, and the details presented herein will facilitate development of envelope as a target for therapeutics and potential chemopreventive agents that could disable the virus before contact with the host cell.
HIV 进入是通过病毒表面包膜蛋白复合物的协同构象变化发生的。该复合物由两个亚基的三聚体异二聚体组成:表面亚基 gp120 和跨膜亚基 gp41。包膜复合物的构象变化使 gp41 介导膜融合,导致两个 gp41 区域的暴露:N-七肽重复(NHR)和 C-七肽重复(CHR)。已经发现 NHR 或 CHR 的肽能够抑制 HIV 的进入。在此,我们通过使用抑制性肽上的共价反应基团,将 gp41 中间体永久性地固定在病毒表面上,从而实现对 HIV 病毒进入的共价抑制。这证明了在 HIV 病毒进入过程中存在脆弱的构象中间体,本文中提供的详细信息将有助于将包膜作为治疗靶点和潜在的化学预防剂进行开发,这些制剂可以在与宿主细胞接触之前使病毒失活。