Objective
Hopes of radical malaria control have been thwarted by the emergence and rapid spread of human malarial parasites that are resistant to every common drug available, including chloroquine, quinine, mefloquine, pyrimethamine, cycloguanil and sulfadoxin. To make matters worse, such multi-drug resistant plasmodium falciparum strains acquire resistances to new antimalarial compounds 1000 times more frequently than do wild-type clones, a phenotype called accelerated resistance to multiple drugs (ARMD), Here we propose a genetic cross to identify the genetic deterministic high level chloroquine drug resistance as well as the accelerated-resistance-to-multiple-drugs phenotype.
Fields of science
Call for proposal
Data not availableFunding Scheme
CSC - Cost-sharing contractsCoordinator
69120 Heidelberg
Germany