Boler-ParseghianCenter for Rare and Neglected Diseases, University of Notre Dame, 103 Galvin Life Sciences, Notre Dame, Indiana 46556, USA.
Department of Biological Sciences, University of Notre Dame, 103 Galvin Life Sciences, Notre Dame, Indiana 46556, USA.
Nat Rev Microbiol. 2018 Mar;16(3):156-170. doi: 10.1038/nrmicro.2017.161. Epub 2018 Jan 22.
A marked decrease in malaria-related deaths worldwide has been attributed to the administration of effective antimalarials against Plasmodium falciparum, in particular, artemisinin-based combination therapies (ACTs). Increasingly, ACTs are also used to treat Plasmodium vivax, the second major human malaria parasite. However, resistance to frontline artemisinins and partner drugs is now causing the failure of P. falciparum ACTs in southeast Asia. In this Review, we discuss our current knowledge of markers and mechanisms of resistance to artemisinins and ACTs. In particular, we describe the identification of mutations in the propeller domains of Kelch 13 as the primary marker for artemisinin resistance in P. falciparum and explore two major mechanisms of resistance that have been independently proposed: the activation of the unfolded protein response and proteostatic dysregulation of parasite phosphatidylinositol 3- kinase. We emphasize the continuing challenges and the imminent need to understand mechanisms of resistance to improve parasite detection strategies, develop new combinations to eliminate resistant parasites and prevent their global spread.
全球疟疾相关死亡人数的显著下降归因于针对恶性疟原虫(尤其是青蒿素为基础的联合疗法)的有效抗疟药物的使用。青蒿素类复方疗法(ACTs)也越来越多地用于治疗第二种主要的人类疟原虫——间日疟原虫。然而,青蒿素类药物和联合用药的一线药物耐药性正在导致东南亚恶性疟原虫青蒿素类复方疗法的失败。在这篇综述中,我们讨论了我们目前对青蒿素类药物和 ACTs 耐药性的标志物和机制的认识。特别是,我们描述了Kelch13 螺旋桨结构域突变作为恶性疟原虫青蒿素耐药性的主要标志物的鉴定,并探讨了已独立提出的两种主要耐药机制:未折叠蛋白反应的激活和寄生虫磷脂酰肌醇 3-激酶的蛋白质稳态失调。我们强调了持续存在的挑战和迫切需要了解耐药机制,以改进寄生虫检测策略、开发新的组合来消除耐药寄生虫并防止其在全球传播。