论文部分内容阅读
HIV-1通过其包膜糖蛋白跨膜亚基gp41介导的病毒-细胞膜融合进入和感染靶细胞.HIV-1融合抑制剂以gp41为靶点,通过阻断病毒与宿主细胞膜的融合,在感染的初始环节切断HIV-1的复制周期.2003年,首个多肽类融合抑制剂T-20获美国食品药物管理局(FDA)批准上市,但其易被体内蛋白酶降解、临床剂量大、耐受性差,且耐药性HIV-1毒株也很快出现.针对这些缺点,近年来在融合抑制剂的作用机制研究和新融合抑制剂的研发等方面取得了重要进展.以gp41不同功能区为靶点,具有高活性和更好代谢性质的多肽及多肽类似物候选分子不断被发现,成为抗HIV药物研究领域的热点之一.本文综述了多肽和类肽类融合抑制剂的研究进展,为相关的药物开发和基础研究提供参考.
HIV-1 enters and infects target cells through virus-cell membrane fusion mediated by its envelope glycoprotein gp41, and HIV-1 fusion inhibitor targets gp41 by blocking the fusion of the virus with the host cell membrane, The initial link of infection was to cut off the replication cycle of HIV-1. In 2003, the first peptide fusion inhibitor, T-20, was approved by the US Food and Drug Administration (FDA) but was easily degraded by proteases in vivo with large clinical doses In recent years, significant progress has been made in the study of the mechanism of fusion inhibitors and the development of new fusion inhibitors.Using gp41 different functional regions As a target, candidate peptides of polypeptide and polypeptide analogues with high activity and better metabolic properties are continuously discovered and become one of the hottest fields in the field of anti-HIV drug research.In this paper, the research progress of peptide and peptoid fusion inhibitors are reviewed, For related drug development and basic research provide a reference.