Here are presented recent studies on this potential antimalarial target, utilising the rodent P. berghei model to investigate the physiological importance of D-glucose transport in transmission and liver life cycle stages and to generate an in vivo model for testing inhibitors of PfHT.
Protozoan parasites that cause malaria export hundreds of proteins into their host red blood cell cytosol, and some even beyond that to the extracellular environment.
The concept of a malaria vaccine has sparked great interest for decades; however, the challenge is proving to be a difficult one.
Here, we combine in vivo experimental evolution, a rapid genetic strategy and whole genome re-sequencing to identify the precise genetic basis of artemisinin resistance in a lineage of the rodent malaria parasite, Plasmodium chabaudi.
To determine the frequency of co-infections with Plasmodium species in southern Myanmar, we investigated the prevalence of P. knowlesi.
Our results suggest that FIKK members phosphorylate different membrane skeleton proteins of the infected erythrocyte in a stage-specific manner, inducing alterations in the mechanical properties of the parasite-infected red blood cell.
In conclusion, this study suggests the existence of serologically distinct VSACM and VSAUM. CM isolates were shown to share common epitopes. Specific antibody response to VSAUM was predominant, suggesting a relative low diversity of VSAUM in the study area.
A recent study in BMC Genetics has found that populations of the malaria parasite Plasmodium vivax should be amenable to GWAS searching for a genetic basis of parasite pathogenicity.
Genetic engineering provides an ingenious method of attenuating Plasmodium falciparum parasites for next generation vaccines.
This Phase 2 trial of a bivalent AMA1 malaria vaccine found no evidence of vaccine selection or strain-specific efficacy, suggesting that the extreme genetic diversity of AMA1 did not account for failure of the vaccine to provide protection.