TY - JOUR
T1 - Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking
AU - Henriques, Gisela
AU - Martinelli, Axel
AU - Rodrigues, Louise
AU - Modrzynska, Katarzyna
AU - Fawcett, Richard
AU - Houston, Douglas R
AU - Borges, Sofia T
AU - d'Alessandro, Umberto
AU - Tinto, Halidou
AU - Karema, Corine
AU - Hunt, Paul
AU - Cravo, Pedro
PY - 2013
Y1 - 2013
N2 - 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.
AB - 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.
U2 - 10.1186/1475-2875-12-118
DO - 10.1186/1475-2875-12-118
M3 - Article
C2 - 23561245
SN - 1475-2875
VL - 12
JO - Malaria Journal
JF - Malaria Journal
M1 - 118
ER -