The data suggest that persistence of PfHRP2 is due to slower clearance of protein from the RBC fraction of the whole blood.
The global emergence of drug resistance in malaria is impeding the therapeutic efficacy of existing antimalarial drugs.
The combination of CPE with the artemisinin derivatives were safe in the rodent model and showed a synergistic anti-malarial activity in vivo and in vitro.
Gametocytes are nonreplicative sexual forms that mediate malaria transmission to a mosquito vector.
We investigated in a murine model the protective efficacy and immune responses after ID or IV immunization of sporozoites.
In tropical regions, protozoan parasites can cause severe diseases with malaria, leishmaniasis, sleeping sickness, and Chagas disease standing in the forefront.
These results suggest that memory CD8+ T cells can be established postinfection with P. berghei ANKA, but their recall responses during reinfection are more profoundly inhibited than responses of naive CD8+ T cells.
Here, we investigate this in Plasmodium berghei by crossing a PbLAP1 null mutant parasite with a parasite line expressing GFP-tagged PbLAP3 that displays strong fluorescence in gametocytes.
These results suggest that malaria parasite may switch the energy metabolism from glycolysis to oxidative phosphorylation to adapt to the insect vector where glucose is not readily available for ATP production.
New drugs to treat malaria must act rapidly and be highly potent against asexual blood stages, well tolerated, and affordable to residents of regions of endemicity.
