Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum infection

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Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum infection

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Title: Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum infection
Author: Cserti-Gazdewich, Christine M; Dhabangi, Aggrey; Musoke, Charles; Ssewanyana, Isaac; Ddungu, Henry; Nakiboneka-Ssenabulya, Deborah; Nabukeera-Barungi, Nicolette; Mpimbaza, Arthur; Dzik, Walter Henry

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Citation: Cserti-Gazdewich, Christine M, Aggrey Dhabangi, Charles Musoke, Isaac Ssewanyana, Henry Ddungu, Deborah Nakiboneka-Ssenabulya, Nicolette Nabukeera-Barungi, Arthur Mpimbaza, and Walter H Dzik. 2012. Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum infection. British Journal of Haematology 159(2): 223-236.
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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.
Published Version: doi:10.1111/bjh.12014
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470923/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10512168
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