Pasupureddy Rahul, Seshadri Sriram, Pande Veena, Dixit Rajnikant, Pandey Kailash C
National Institute of Malaria Research, Dwarka Sector 8, New Delhi, 110077, India.
Institute of Science, Nirma University, SG Highway, Ahmedabad, Gujarat, 382481, India.
Parasitol Res. 2019 Jan;118(1):29-42. doi: 10.1007/s00436-018-6126-x. Epub 2018 Nov 26.
Despite several setbacks in the fight against malaria such as insecticide and drug resistance as well as low efficacy of available vaccines, considerable success in reducing malaria burden has been achieved in the past decade. Artemisinins (ARTs and their combination therapies, ACTs), the current frontline drugs against uncomplicated malaria, rapidly kill plasmodial parasites and are non-toxic at short exposures. Though the exact mode of action remains unclear, the endoperoxide bridge, indispensable for ART activity, is thought to react with heme released from hemoglobin hydrolysis and generate free radicals that alkylate multiple protein targets, thereby disrupting proteostasis pathways. However, rapid development of ART resistance in recent years with no potential alternatives on the horizon threaten the elimination efforts. The Greater Mekong Subregion in South-East Asia continues to churn out mutants resistant to multiple ACTs and detected in increasingly expanding geographies. Extensive research on ART-resistant strains have identified a potential candidate Kelch13, crucial for mediating ART resistance. Parasites with mutations in the propeller domains of Plasmodium falciparum Kelch13 protein were shown to have enhanced phosphatidylinositol 3-kinase levels that were concomitant with delayed parasite clearance. Current research focused on understanding the mechanism of Kelch13-mediated ART resistance could provide better insights into Plasmodium resistome. This review covers the current proposed mechanisms of ART activity, resistance strategies adopted by the parasite in response to ACTs and possible future approaches to mitigate the spread of resistance from South-East Asia.
尽管在抗击疟疾的斗争中遭遇了一些挫折,如杀虫剂和药物耐药性以及现有疫苗的低效力,但在过去十年中,在减轻疟疾负担方面已经取得了相当大的成功。青蒿素(ARTs及其联合疗法,ACTs)是目前治疗非复杂性疟疾的一线药物,能迅速杀死疟原虫寄生虫,且短时间接触无毒。尽管确切的作用方式仍不清楚,但对于ART活性不可或缺的内过氧化物桥,被认为与血红蛋白水解释放的血红素反应并产生自由基,这些自由基使多个蛋白质靶点烷基化,从而破坏蛋白质稳态途径。然而,近年来ART耐药性的迅速发展且暂无潜在替代药物,这威胁到了消除疟疾的努力。东南亚的大湄公河次区域持续出现对多种ACTs耐药的突变体,且在越来越多的地区被检测到。对ART耐药菌株的广泛研究已经确定了一个潜在的候选基因Kelch13,它对于介导ART耐药性至关重要。恶性疟原虫Kelch13蛋白螺旋桨结构域发生突变的寄生虫显示出磷脂酰肌醇3激酶水平升高,这与寄生虫清除延迟同时出现。目前专注于理解Kelch13介导的ART耐药性机制的研究,可能会为疟原虫耐药组提供更好的见解。本综述涵盖了目前提出的ART活性机制、寄生虫针对ACTs采取的耐药策略以及未来减轻东南亚耐药性传播的可能方法。