University of California, Merced, California 95343, USA.
J Biol Chem. 2011 Aug 12;286(32):28370-81. doi: 10.1074/jbc.M111.234799. Epub 2011 Jun 9.
Blocking HIV-1 cell entry has long been a major goal of anti-HIV drug development. Here, we report a successful design of two highly potent chimeric HIV entry inhibitors composed of one CCR5-targeting RANTES (regulated on activation normal T cell expressed and secreted) variant (5P12-RANTES or 5P14-RANTES (Gaertner, H., Cerini, F., Escola, J. M., Kuenzi, G., Melotti, A., Offord, R., Rossitto-Borlat, I., Nedellec, R., Salkowitz, J., Gorochov, G., Mosier, D., and Hartley, O. (2008) Proc. Natl. Acad. Sci. U.S.A. 105, 17706-17711)) linked to a gp41 fusion inhibitor, C37. Chimeric inhibitors 5P12-linker-C37 and 5P14-linker-C37 showed extremely high antiviral potency in single cycle and replication-competent viral assays against R5-tropic viruses, with IC(50) values as low as 0.004 nm. This inhibition was somewhat strain-dependent and was up to 100-fold better than the RANTES variant alone or in combination with unlinked C37. The chimeric inhibitors also fully retained the antiviral activity of C37 against X4-tropic viruses, and this inhibition can be further enhanced significantly if the target cell co-expresses CCR5 receptor. On human peripheral blood mononuclear cells, the inhibitors showed very strong inhibition against R5-tropic Ba-L strain and X4-tropic IIIB strain, with IC(50) values as low as 0.015 and 0.44 nm, which are 45- and 16-fold better than the parent inhibitors, respectively. A clear delivery mechanism requiring a covalent linkage between the two segments of the chimera was observed and characterized. Furthermore, the two chimeric inhibitors are fully recombinant and are easily produced at low cost. These attributes make them excellent candidates for anti-HIV microbicides. The results of this study also suggest a potent approach for optimizing existing HIV entry inhibitors or designing new inhibitors.
阻断 HIV-1 细胞进入一直是抗 HIV 药物开发的主要目标。在这里,我们报告了两种高效的嵌合 HIV 进入抑制剂的成功设计,它们由一种 CCR5 靶向 RANTES(激活正常 T 细胞表达和分泌的调节)变体(5P12-RANTES 或 5P14-RANTES(Gaertner,H.,Cerini,F.,Escola,J.M.,Kuenzi,G.,Melotti,A.,Offord,R.,Rossitto-Borlat,I.,Nedellec,R.,Salkowitz,J.,Gorochov,G.,Mosier,D.,和 Hartley,O.(2008)Proc. Natl. Acad. Sci. U.S.A. 105, 17706-17711))与 gp41 融合抑制剂 C37 相连。嵌合抑制剂 5P12-linker-C37 和 5P14-linker-C37 在单周期和复制性病毒测定中对 R5 嗜性病毒表现出极高的抗病毒效力,IC(50)值低至 0.004nm。这种抑制作用有些依赖于病毒株,比单独的 RANTES 变体或与未连接的 C37 联合使用要好 100 倍。嵌合抑制剂还完全保留了 C37 对 X4 嗜性病毒的抗病毒活性,如果靶细胞共表达 CCR5 受体,这种抑制作用可以显著增强。在人外周血单核细胞上,抑制剂对 R5 嗜性 Ba-L 株和 X4 嗜性 IIIB 株表现出很强的抑制作用,IC(50)值低至 0.015 和 0.44nm,分别比亲本抑制剂好 45 倍和 16 倍。观察到并表征了一种需要嵌合体两个片段之间形成共价键的明确传递机制。此外,这两种嵌合抑制剂都是完全重组的,并且可以低成本轻松生产。这些特性使它们成为抗 HIV 杀微生物剂的优秀候选物。该研究的结果还表明了一种优化现有 HIV 进入抑制剂或设计新抑制剂的有效方法。