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Plasmodium falciparum malaria remains a significant cause of human suffering, and most malaria-related morbidity and mortality occurs in children living in sub-Sahara Africa. Evolutionary pressure has explained that various erythrocyte polymorphisms could protect against severe complications and death from Plasmodium falciparum malaria. Several mechanisms have been proposed to explain the protection of hemoglobin AS and SS from severe Plasmodium falciparum malaria. Sickle trait; the heterozygous and homozygous state of normal hemoglobin A (HbA) could confer protection against malaria in Africa. In the present study, we cultured Plasmodium falciparum infected red blood cells from AA, AS and SS for six days. During the six days period, the level of parasite load (Parasitemia) and the activity of arginase released by the parasite were monitored on daily basis. Result obtained shows a significant (P<0.05) increase in both the level of parasite load and the activity of arginase. This increase was found to be higher in AA genotype while lower in both SS and AS, but with AS been much lower. The mechanisms by which sickle trait confer such malaria protection might be as a result of change in structural conformation that alter with the parasite ability to invade into the cells through the membrane protein receptors and hence a decrease in its activity in both AS and SS respectively.

Genotypic Variations may Elucidate Resistance to Plasmodium falciparum Infection In Vitro