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Published on: May 16, 2013
Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum
Christine M Cserti-Gazdewich1, Aggrey Dhabangi, Charles Musoke
1University Health Network/University of Toronto, Ontario, Canada. christine.cserti@uhn.ca
Insights
Blood group O and specific host receptors like CD36 and ICAM1 offer survival advantages against severe malaria in children. These genetic factors are crucial for understanding malaria pathogenesis and developing new treatments.
Area of Science:
- Genetics and Molecular Biology
- Immunology
- Tropical Medicine
Background:
- Plasmodium falciparum malaria is a major global cause of childhood mortality.
- Severe malaria involves microcirculation disturbances due to infected erythrocyte adhesion to host receptors.
Purpose of the Study:
- To compare host cytoadhesion receptor expression in children with uncomplicated versus severe malaria.
- To identify host genetic factors associated with malaria severity and survival.
Main Methods:
- Prospective study of Ugandan children with uncomplicated and severe malaria (cerebral malaria, severe anemia, lactic acidosis).
- Comparison of major host cytoadhesion receptor expression (CD36, ICAM1) and blood groups.
- Logistic regression analysis to model disease severity.
Main Results:
- Blood group O, increased monocyte CD36, and ICAM1 expression were linked to a survival advantage.
- Severe malaria syndromes (cerebral malaria, lactic acidosis) associated with high platelet CD36 and thrombocytopenia.
- Severe malaria anemia linked to low ICAM1 expression.
- Genetic factors (blood group O, CD36, ICAM1) showed stronger protective effects than sickle hemoglobin.
Conclusions:
- Host genetic factors significantly influence malaria outcomes.
- CD36 and ICAM1 expression patterns correlate with specific severe malaria manifestations.
- Host genetic adaptations present potential targets for novel malaria therapies.
Abstract:
As a leading cause of childhood mortality worldwide, selection pressure by Plasmodium falciparum continues 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 group O and increased monocyte expression of CD36 and ICAM1 (CD54). The high case fatality rate syndromes of cerebral malaria and lactic acidosis were associated with high platelet CD36 expression and thrombocytopenia, and severe malaria anaemia was characterized by low ICAM1 expression. In a logistic regression model of disease severity, odds ratios for the mitigating effects of blood group O, CD36, and ICAM1 phenotypes were greater than that of sickle haemoglobin. Host genetic adaptations to Plasmodium falciparum suggest new potential malaria treatment strategies.
