The human immunodeficiency virus type-1 (HIV-1) envelope (Env) proteins that mediate membrane fusion represent a major target for the development of new AIDS therapies. Three classes of Env-mediated membrane fusion inhibitors have been described that specifically target the pre-hairpin intermediate conformation of gp41. Class 2 inhibitors bind to the C-terminal heptad repeat (C-HR) of gp41. The single example of a class 3 inhibitor targets the trimeric N-terminal heptad repeat (N-HR) of gp41 and has been postulated to sequestrate the N-HR of the pre-hairpin intermediate through the formation of fusion incompetent heterotrimers. Here, we show that N(CCG)-gp41, a class 2 inhibitor, and N36(Mut(e,g)), a class 3 inhibitor, synergistically inhibit Env-mediated membrane fusion for several representative HIV-1 strains (X4 and R5) in both a cell fusion assay (with membrane-bound CD4) and an Env-pseudo-typed virus neutralization assay. The mechanistic, as well as potential therapeutic, implications of these observations for HIV-Env-mediated membrane fusion are discussed.

译文

:介导膜融合的人类1型免疫缺陷病毒(HIV-1)包膜(Env)蛋白代表了开发新的AIDS疗法的主要目标。已经描述了三类Env介导的膜融合抑制剂,它们专门针对gp41的发夹前中间体构象。 2类抑制剂与gp41的C端七肽重复序列(C-HR)结合。第3类抑制剂的单个实例靶向gp41的三聚体N端七末端重复序列(N-HR),并已假定通过形成不适合的融合三聚体来隔离发夹前中间体的N-HR。在这里,我们显示N(CCG)-gp41(一种2类抑制剂)和N36(Mut(e,g))(一种3类抑制剂)协同抑制Env介导的几种代表性HIV-1菌株的膜融合(X4和R5)在细胞融合测定(带有膜结合CD4)和Env-伪型病毒中和测定中都可以使用。讨论了这些观察结果对HIV-Env介导的膜融合的机理以及潜在的治疗意义。

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