摘要
疟疾是严重威胁人类健康的主要传染病之一。尽管以青蒿素为基础的青蒿素联合疗法(ACT)能有效控制疟疾扩散及降低疟疾死亡率,但近年来不断发现的恶性疟原虫对青蒿素和ACT的耐药性引起了广泛的关注。通过回顾相关文献,本文综述了恶性疟原虫多药耐药性基因(Pfmdr1)、恶性疟原虫氯喹耐药性转运蛋白基因(Pfcrt)、恶性疟原虫钙ATP蛋白6基因(Pfatp6)和恶性疟原虫K13基因(Pfkelch13)及其他青蒿素耐药性机制的研究,为进一步探索疟原虫青蒿素耐药分子机制和监控耐药疟原虫的扩散提供参考。
Malaria is one of the main infectious diseases threatening human health worldwide. Despite the effective control of malaria spread and reduction of mortality by artemisinin-based combination therapy (ACT), Plasmodium falciparum resistance to artemisinin and ACT is increasingly found in recent years. The present review summarizes the molecular mechanisms of artemisinin resistance in P. falciparum including the roles of genes P. falciparum multidrug resistance 1(Pfmdr1), P. falciparum chloroquine resistance transporter (Pfcrt), P. falciparum calcium ATPase 6(Pfatp6), and Pfkelch13, in order to advance our understanding of molecular mechanisms of artemisinin resistance and provide reference for the control and surveillance of spread of artemisinin-resistant malaria parasites.
出处
《中国寄生虫学与寄生虫病杂志》
CAS
CSCD
北大核心
2018年第6期636-642,共7页
Chinese Journal of Parasitology and Parasitic Diseases
基金
国家重点研究和发展项目(No.2016YFC1202003,N0.2016YFC1202005)
国家自然科学基金(No.81641094)
广东省自然科学基金(No.S2012010008504)
高等学校学科创新引智计划(No.B12003).
关键词
青蒿素
疟疾
分子机制
耐药
恶性疟原虫
Artemisinin
Malaria
Molecular mechanism
Drug resistance
Plasmodium falciparum
