Cytoadherence in paediatric malaria:ABOblood group,CD36, andICAM1 expression and severePlasmodium falciparuminfection
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SummaryAs a leading cause of childhood mortality worldwide, selection pressure byPlasmodium falciparumcontinues to shape the human genome. Severe disturbances within the microcirculation result from the adhesion of infected erythrocytes to host receptors on monocytes, platelets, and endothelium. In this prospective study, we compared expression of all major host cytoadhesion receptors among Ugandan children presenting with uncomplicated malaria (n = 1078) versus children with severe malaria (n = 855), including cerebral malaria (n = 174), severe anaemia (n = 522), and lactic acidosis (n = 154). We report a significant survival advantage attributed to blood groupOand increased monocyte expression ofCD36 andICAM1 (CD54). The high case fatality rate syndromes of cerebral malaria and lactic acidosis were associated with high plateletCD36 expression and thrombocytopenia, and severe malaria anaemia was characterized by lowICAM1 expression. In a logistic regression model of disease severity, odds ratios for the mitigating effects of blood groupO,CD36, andICAM1 phenotypes were greater than that of sickle haemoglobin. Host genetic adaptations toPlasmodium falciparumsuggest new potential malaria treatment strategies.
