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

ABSTRACT:

Background

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.

Methods

Here, for a mutant P. chabaudi malaria parasite and its immediate progenitor, the in vivo artemisin

SUBMITTER: Henriques G 

PROVIDER: S-EPMC3655824 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature