中国寄生虫学与寄生虫病杂志 ›› 2018, Vol. 36 ›› Issue (6): 636-642.

• 综述 • 上一篇    下一篇

疟原虫青蒿素耐药分子机制探索

牟畇珊, 李璐杰, 吴银娟, 李学荣*()   

  1. 中山大学中山医学院寄生虫学教研室,教育部热带病防治重点实验室,广东省生物媒介控制工程技术研究开发中心,广州 510080
  • 收稿日期:2018-04-25 出版日期:2018-12-30 发布日期:2019-01-08
  • 通讯作者: 李学荣
  • 基金资助:
    国家重点研究和发展项目(No. 2016YFC1202003,No. 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)

Exploration of molecular mechanisms of artemisinin resistance in malaria parasites

Yun-shan MOU, Lu-jie LI, Yin-juan WU, Xue-rong LI*()   

  1. Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University
    Key Laboratory of Tropical Disease Control, Chinese Ministry of Education
    Provincial Engineering Technology Research Center for Biological Vector Control, Guangzhou 510080, China
  • Received:2018-04-25 Online:2018-12-30 Published:2019-01-08
  • Contact: Xue-rong LI
  • Supported by:
    Supported by the National Key Research and Development Program of China(No. 2016YFC1202003, No. 2016YFC1202005), the National Natural Science Foundation of China(No. 81641094), the Guangdong Natural Science Foundation(No. S2012010008504), and the Programme of Overseas Expertise Introduction Project for Discipline Innovation(No. B12003)

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。

关键词: 青蒿素, 疟疾, 分子机制, 耐药, 恶性疟原虫

Abstract:

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.

Key words: Artemisinin, Malaria, Molecular mechanism, Drug resistance, Plasmodium falciparum

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