An appraisal of the best known erythrocytic genetic adaptations of man to malaria and its implications

Cytoadherence in paediatric malaria:ABOblood group,CD36, andICAM1 expression and severePlasmodium falciparuminfection

“…Prior to developing adaptive immunity and gaining access to therapy, malaria-infected children depend upon host attributes that optimize parasite clearance or mitigate lethal pathophysiology (Stevenson & Riley, 2004 ). The best appreciated adaptations to P. falciparum , such as sickle haemoglobin and thalassaemia, appear to be concerned not with invasion resistance, but rather with earlier clearance of infected erythrocytes (iRBC) within the spleen as a result of modified red cell fitness (Modiano, 1998 ). Furthermore, the most lethal malaria syndromes appear to associate with enhanced iRBC adhesion (Miller et al , 2002 ; Rowe et al , 2009a ), wherein parasite traffic to the spleen is reduced by systemic (“extrasplenic”) sequestration of iRBC.…”