C57BL/6 mice infected with Plasmodium berghei ANKA (PbA) develop neurological symptoms and die 6-–7-day post-inoculation in the absence of high parasitemia.
The complex life cycle of malaria parasites requires well-orchestrated stage specific gene expression. In the vertebrate host the parasites grow and multiply by schizogony in two different environments: within erythrocytes and within hepatocytes. Whereas erythrocytic parasites are well-studied in this respect, relatively little is known about the exo-erythrocytic stages.
Reverse genetics approaches have become powerful tools to dissect the biology of malaria parasites. In a previous study, development of an in vitro drug selection method for generating transgenic parasite of Plasmodium berghei was reported. Using this method, two novel and independent selection markers using the P. berghei heat shock protein 70 promoter was previously established. While the approach permits the easy and flexible genetic manipulation of P. berghei, shortcomings include a low variety in promoter options to drive marker gene expression and increased complexity of the selection procedure. In this study, addressing these issues was attempted.
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.