Centre for Molecular Pathogenesis, Retrovirus and Associated Infections Unit (URIA-CPM), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.
AIDS Rev. 2013 Jan-Mar;15(1):49-61.
Currently, there is a growing interest in using entry inhibitors to treat HIV-2-infected patients because, among the available drugs, few are fully active against HIV-2. Recent studies indicate that maraviroc and other experimental entry inhibitors, including new CCR5 and CXCR4 antagonists, inhibit primary isolates of HIV-2 as well as HIV-1 and may, therefore, expand the existing therapeutic armamentarium against HIV-2. There are, however, significant differences between the evolution of HIV-1 and HIV-2 envelope glycoproteins during infection that can lead to differences in the response to therapy with entry inhibitors over the course of the infection. Here, we review the available data on the susceptibility of HIV-2 to entry inhibitors in the context of the evolution of the sequence, structure, and function of envelope glycoproteins during infection.
目前,人们越来越感兴趣地使用进入抑制剂来治疗感染 HIV-2 的患者,因为在现有药物中,很少有药物能完全有效地对抗 HIV-2。最近的研究表明,马拉维若和其他实验性进入抑制剂,包括新的 CCR5 和 CXCR4 拮抗剂,不仅能抑制 HIV-1 原代分离物,而且还能抑制 HIV-2,因此可能扩大现有的针对 HIV-2 的治疗手段。然而,在感染过程中,HIV-1 和 HIV-2 包膜糖蛋白的进化存在显著差异,这可能导致在感染过程中对进入抑制剂治疗的反应存在差异。在此,我们根据包膜糖蛋白在感染过程中序列、结构和功能的演变,综述了现有的 HIV-2 对进入抑制剂敏感性的数据。