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恶性疟原虫对青蒿素类复方疗法的抗药性。

Plasmodium falciparum resistance to artemisinin-based combination therapies.

机构信息

Department of Microbiology and Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.

Department of Microbiology and Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA; Center for Malaria Therapeutics and Antimicrobial Resistance, Division of Infectious Diseases, Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA.

出版信息

Curr Opin Microbiol. 2022 Oct;69:102193. doi: 10.1016/j.mib.2022.102193. Epub 2022 Aug 22.

Abstract

Multidrug-resistant Plasmodium falciparum parasites are a major threat to public health in intertropical regions. Understanding the mechanistic basis, origins, and spread of resistance can inform strategies to mitigate its impact and reduce the global burden of malaria. The recent emergence in Africa of partial resistance to artemisinins, the core component of first-line combination therapies, is particularly concerning. Here, we review recent advances in elucidating the mechanistic basis of artemisinin resistance, driven primarily by point mutations in P. falciparum Kelch13, a key regulator of hemoglobin endocytosis and parasite response to artemisinin-induced stress. We also review resistance to partner drugs, including piperaquine and mefloquine, highlighting a key role for plasmepsins 2/3 and the drug and solute transporters P. falciparum chloroquine-resistance transporter and P. falciparum multidrug-resistance protein-1.

摘要

耐多药恶性疟原虫寄生虫对热带地区的公共卫生是一个主要威胁。了解耐药性的机制基础、起源和传播可以为减轻其影响和降低全球疟疾负担的策略提供信息。最近在非洲出现的对青蒿素部分耐药性,这是一线联合疗法的核心成分,尤其令人担忧。在这里,我们回顾了阐明青蒿素耐药性机制基础的最新进展,这主要是由恶性疟原虫 Kelch13 中的点突变驱动的,Kelch13 是血红蛋白内吞作用和寄生虫对青蒿素诱导的应激反应的关键调节剂。我们还回顾了对联合用药的耐药性,包括哌喹和甲氟喹,突出了疟原虫蛋白酶 2/3 和药物及溶质转运蛋白恶性疟原虫氯喹耐药转运蛋白和恶性疟原虫多药耐药蛋白 1 的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0658/9847095/a97239ddb89f/nihms-1864674-f0001.jpg

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