Falciparum malaria appears to be a selective pressure keeping Hb S frequencies high; yet it may not be the major selective force maintaining the G6PD polymorphism.
The effect of X chromosome inactivation on the inhibition of Plasmodium falciparum malaria growth by glucose-6-phosphate-dehydrogenase-deficient red cells.
Erythrocyte 6-phosphogluconate dehydrogenase A (PGDA) and phosphoglucomutase 1 (PGM1), phenotypes of unknown relevance to protection against falciparum malaria, were also significantly more prevalent in those claiming resistance to malaria.
Therefore, the level of expression of CD36 on normal RBCs is sufficient to be important in cell adherence, and may have a biologic role in normal individuals as well as in the pathology of P falciparum malaria.
As chloroquine resistance spreads across Africa, the dihydrofolate reductase (DHFR) inhibitors pyrimethamine and proguanil are being used as alternative first-line drugs for the treatment and prevention of Plasmodium falciparum malaria.
The effect of antiparasitic therapy on the induction of TF by serum from patients with complicated P. falciparum malaria is dependent on a therapy-mediated loss of activation of NF-kappa B-like proteins in post-treatment patient serum.
Tumor necrosis factor in Plasmodium falciparum malaria: high plasma level is associated with fever, but high production capacity is associated with rapid fever clearance.
In conclusion, the results of this study suggest that parasite antigen-specific IL-10-mediated antibody responses may play a role in the control of asexual stage parasite multiplication in P. falciparum malaria.
The increasing resistance of falciparum malaria to common antimalarial drugs has renewed interest in the compound proguanil normally metabolized to cycloguanil, a strong dihydrofolate reductase inhibitor, via the cytochrome P450 isozyme CYP2C19.
To assess pyrimethamine-sulfadoxine (PS) efficacy in Mali, and the role of mutations in Plasmodium falciparum dihydrofolate reductase (DHFR) and dihydropteroate synthase (DHPS) in in vivo PS resistance, 190 patients with uncomplicated P. falciparum malaria were treated with PS and monitored for 56 days.
Here, we present an analysis of four published data sets for vector-borne microparasite infections where strains or genotypes have been distinguished: serotypes of African horse sickness (AHS) in zebra; types of Nannomonas trypanosomes in tsetse flies; parasite-induced erythrocyte surface antigen (PIESA) based isolates of Plasmodium falciparum malaria in humans, and the merozoite surface protein 2 gene (MSP-2) alleles of P. falciparum in humans and in anopheline mosquitoes.
Here, we present an analysis of four published data sets for vector-borne microparasite infections where strains or genotypes have been distinguished: serotypes of African horse sickness (AHS) in zebra; types of Nannomonas trypanosomes in tsetse flies; parasite-induced erythrocyte surface antigen (PIESA) based isolates of Plasmodium falciparum malaria in humans, and the merozoite surface protein 2 gene (MSP-2) alleles of P. falciparum in humans and in anopheline mosquitoes.
Here, we present an analysis of four published data sets for vector-borne microparasite infections where strains or genotypes have been distinguished: serotypes of African horse sickness (AHS) in zebra; types of Nannomonas trypanosomes in tsetse flies; parasite-induced erythrocyte surface antigen (PIESA) based isolates of Plasmodium falciparum malaria in humans, and the merozoite surface protein 2 gene (MSP-2) alleles of P. falciparum in humans and in anopheline mosquitoes.
Here, we present an analysis of four published data sets for vector-borne microparasite infections where strains or genotypes have been distinguished: serotypes of African horse sickness (AHS) in zebra; types of Nannomonas trypanosomes in tsetse flies; parasite-induced erythrocyte surface antigen (PIESA) based isolates of Plasmodium falciparum malaria in humans, and the merozoite surface protein 2 gene (MSP-2) alleles of P. falciparum in humans and in anopheline mosquitoes.
Sequence variations in the genes encoding dihydropteroate synthase and dihydrofolate reductase and clinical response to sulfadoxine-pyrimethamine in patients with acute uncomplicated falciparum malaria.