Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking

Gisela Henriques, Axel Martinelli, Louise Rodrigues, Katarzyna Modrzynska, Richard Fawcett, Douglas R Houston, Sofia T Borges, Umberto d'Alessandro, Halidou Tinto, Corine Karema, Paul Hunt, Pedro Cravo

Research output: Contribution to journalArticlepeer-review

Abstract

The control of malaria, caused by Plasmodium falciparum, is hampered by the relentless evolution of drug resistance. Because artemisinin derivatives are now used in the most effective anti-malarial therapy, resistance to artemisinin would be catastrophic. Indeed, studies suggest that artemisinin resistance has already appeared in natural infections. Understanding the mechanisms of resistance would help to prolong the effective lifetime of these drugs. Genetic markers of resistance are therefore required urgently. Previously, a mutation in a de-ubiquitinating enzyme was shown to confer artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi.
Original languageEnglish
Article number118
JournalMalaria Journal
Volume12
DOIs
Publication statusPublished - 2013

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