Malarial dihydrofolate reductase (DHFR) is the target of antifolate antimalarial drugs such as pyrimethamine and cycloguanil, the clinical efficacy of which have been compromised by resistance arising through mutations at various sites on the enzyme.
We show that there is no significant population structure among these Senegal sampling sites. By fitting demographic models to the synonymous allele-frequency spectrum, we also estimated a major 60-fold population expansion of this parasite population ∼20,000–40,000 years ago.
We discuss the value of deep population-specific genomic analyses for identifying selection signals within sampled endemic populations of parasites, which may correspond to local selection pressures such as distinctive therapeutic regimes or mosquito vectors.
The host mechanisms responsible for protection against malaria remain poorly understood, with only a few protective genetic effects mapped in humans.
Many successful antimicrobial drugs originate from synthetic dyes.
In a genome-wide screen for alpha-helical coiled coil motifs aiming at structurally defined vaccine candidates we identified PFF0165c.
Our data identify for the first time a malaria parasite gene with structural and functional features of recombinases.
Erythrocyte polymorphisms associated with a survival advantage to Plasmodium falciparum infection have undergone positive selection.
Given the tendency for An. rivulorum to be active early in the evening, the presence of P. falciparum in the species, and the potential for the development of pyrethroid resistance, we strongly advocate reconsideration of the latent ability of this species as an epidemiologically important malaria vector.
It is concluded that IL-6 secretion from MDM in response to CS2 IE does not require phagocytosis, whereas secretion of TNF and IL-1beta is dependent on Fcgamma receptor-mediated phagocytosis; for IL-1beta, this occurs by activation of the inflammasome.
