On page 724 of this issue, Yuan et al. (2) confront the issue head-on. Using high-throughput chemical and gene analysis methods, they not only identify potential new antimalarial drugs that could be used in combination to suppress the development of drug resistance but also characterize a common set of genetic loci and genes affected by these molecules.
We derive, analyse and compare two mathematical models, one for an insecticide that kills on exposure, and the other for an insecticide that targets only older mosquitoes.
Resistance to pyrethroid insecticides in the malaria vector Anopheles gambiae is a major threat to malaria control programmes.
Cerebral malaria is the most severe complication of Plasmodium falciparum infection and accounts for a large number of malaria fatalities worldwide.
This study demonstrates that in 2006-2007 chloroquine and SP continued to be used at high rates in many African countries.
In this report, we have reviewed work on the in vivo efficacy and in vitro activity of quinine, and discussed recent data on genetic markers of resistance to this drug.
These data imply that antimalarial drug resistance can result from defective MMR.
IRAC has just published the second edition of the very popular manual “Prevention and Management of Insecticide Resistance in Vectors of Public Health Importance”.
Recent reports suggest that early stages of resistance to artemisinins and/or its partner drugs could be occurring, thus it is timely to briefly review exactly how ACTs slow the origin and spread of resistance and to interpret the threat of resistance within this context.
The kdr L1014S allele has approached fixation in A. gambiae s.s. populations of western Kenya, and these same populations exhibit varying degrees of phenotypic resistance to DDT and pyrethroid insecticides.