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Cytoadherence in paediatric malaria: ABO blood group, CD 36, and ICAM 1 expression and severe P lasmodium falciparum infection
Author(s) -
CsertiGazdewich Christine M.,
Dhabangi Aggrey,
Musoke Charles,
Ssewanyana Isaac,
Ddungu Henry,
NakibonekaSsenabulya Deborah,
NabukeeraBarungi Nicolette,
Mpimbaza Arthur,
Dzik Walter H.
Publication year - 2012
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.12014
Subject(s) - plasmodium falciparum , malaria , cerebral malaria , immunology , cd36 , abo blood group system , biology , platelet , odds ratio , case fatality rate , medicine , endothelial activation , receptor , inflammation , epidemiology
Summary As a leading cause of childhood mortality worldwide, selection pressure by P lasmodium 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 CD 36 and ICAM 1 ( CD 54). The high case fatality rate syndromes of cerebral malaria and lactic acidosis were associated with high platelet CD 36 expression and thrombocytopenia, and severe malaria anaemia was characterized by low ICAM 1 expression. In a logistic regression model of disease severity, odds ratios for the mitigating effects of blood group O , CD 36, and ICAM 1 phenotypes were greater than that of sickle haemoglobin. Host genetic adaptations to P lasmodium falciparum suggest new potential malaria treatment strategies.