Figure 1.
General mechanisms by which hemoglobinopathies may attenuate the pathogenesis of falciparum malaria.
(A) Restriction of red blood cell (RBC) invasion or intraerythrocytic growth, thereby suppressing parasite densities in vivo; (B) interference with parasite-derived mediators of pathogenesis, including those involved in the binding of parasite-infected RBCs (iRBCs) to extracellular host receptors; (C) modulation of innate host defenses to favor protective, anti-inflammatory responses over those that drive pathogenic, pro-inflammatory responses; (D) enhancement of adaptive cell-mediated and humoral immune responses that clear iRBCs from the blood.
Table 1.
The major hemoglobinopathies: epidemiology, molecular pathology, and clinical phenotype.
Table 2.
Studies of P. falciparum invasion of and development in RBCs containing hemoglobin variants.