摘要
基孔肯雅病毒 (CHIKV) 是导致基孔肯雅热 (CHIKF) 的甲病毒 (Togaviridae),其主要特征是严重的多关节痛,通过受感染的埃及伊蚊和伊蚊叮咬传播。白纹蚊。如今,没有获得许可的疫苗或批准的药物来专门治疗这种病毒性疾病。结构病毒蛋白参与其复制周期的关键步骤,例如病毒进入、膜融合、核衣壳组装和病毒出芽。在这种情况下,包膜 E3-E2-E1 糖蛋白复合物可以作为设计新候选药物的目标。在这篇综述中,讨论了 CHIKV 进入机制的各个方面,以提供有助于药物发现过程的见解。此外,还探索了几种天然的、基于天然的和合成的化合物,以及重新利用的药物和虚拟筛选,作为开发 CHIKV 进入抑制剂的替代方案。最后,我们对未通过计算机方法探索的抑制剂进行了补充分析。基于此,发现 Phe118、Val179 和 Lys181 是最常见的残基,分别存在于 89.6、82.7 和 93.1% 的复合物中。最后,讨论了与这些抑制剂和成熟包膜 E3-E2-E1 糖蛋白复合物相互作用相关的一些化学问题,以全世界的科学家提供数据为基础,以支持他们寻找针对这种新兴虫媒病毒的新抑制剂。
关键词: 靶点抑制剂、基孔肯雅病毒、药物化学、药物设计、再利用、天然产物、合成、虚拟筛选、分子对接、频率残基。
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