Valderramos Stephanie G, Fidock David A
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Trends Pharmacol Sci. 2006 Nov;27(11):594-601. doi: 10.1016/j.tips.2006.09.005. Epub 2006 Sep 25.
The ability to treat and control Plasmodium falciparum infection through chemotherapy has been compromised by the advent and spread of resistance to antimalarial drugs. Research in this area has identified the P. falciparum chloroquine resistance transporter (PfCRT) and the multidrug resistance-1 (PfMDR1) transporter as key determinants of decreased in vitro susceptibility to several principal antimalarial drugs. Transfection-based in vitro studies are consistent with clinical findings of an association between mutations in the pfcrt gene and failure of chloroquine treatment, and between amplification of the pfmdr1 gene and failure of mefloquine treatment. Many countries are now switching to artemisinin-based combination therapies. These incorporate partner drugs of which some have an in vitro efficacy that can be modulated by changes in pfcrt or pfmdr1. Here, we summarize investigations of these and other recently identified P. falciparum transporters in the context of antimalarial mode of action and mechanisms of resistance.
通过化疗治疗和控制恶性疟原虫感染的能力因对抗疟药物耐药性的出现和传播而受到损害。该领域的研究已确定恶性疟原虫氯喹抗性转运蛋白(PfCRT)和多药抗性1(PfMDR1)转运蛋白是体外对几种主要抗疟药物敏感性降低的关键决定因素。基于转染的体外研究与临床发现一致,即pfcrt基因突变与氯喹治疗失败之间存在关联,pfmdr1基因扩增与甲氟喹治疗失败之间存在关联。许多国家目前正在转向以青蒿素为基础的联合疗法。这些联合疗法包含辅助药物,其中一些药物的体外疗效可因pfcrt或pfmdr1的变化而受到调节。在此,我们在抗疟作用模式和耐药机制的背景下总结了对这些以及其他最近发现的恶性疟原虫转运蛋白的研究。