Our studies demonstrate that skin exoerythrocytic stages are susceptible to destruction in immunized mice, suggesting that their aberrant location does not protect them from the host's adaptive immune response.
Malaria is a serious parasitic disease in the developing world, causing high morbidity and mortality.
6-Oxopurine acyclic nucleoside phosphonates (ANPs) have been shown to be potent inhibitors of hypoxanthine-guanine-xanthine phosphoribosyltransferase (HGXPRT), a key enzyme of the purine salvage pathway in human malarial parasites.
Preventing disease is a major goal of applied bioscience and explaining variation in the harm caused by parasites, and their infectiousness, are major goals of evolutionary biology.
Genetic manipulation of malaria parasites remains an inefficient, time-consuming and resource-intensive process.
We show that var introns can control this process and that var intron addition relocalizes episomes from a random to a perinuclear position.
The diagnosis and treatment of malaria infection requires detecting the presence of the malaria parasite in the patient as well as identification of the parasite species.
Genes underlying important phenotypic differences between Plasmodium species, the causative agents of malaria, are frequently found in only a subset of species and cluster at dynamically evolving subtelomeric regions of chromosomes.
Our data show the surface expression of non-functional PfEMP1 in D10 strongly indicating that genes other than clag9 deleted from chromosome 9 are involved in this virulence process possibly via post-translational modifications.
Here, we review recent studies on interactions between erythrocyte binding antigens (EBA) and PfRH proteins from the parasite and erythrocyte receptors involved in invasion.