Blankson, S.O.Dadjé, D.S.Traikia, N.Alao, M.J.Ayivi, S.Amoussou, A.Deloron, P.Ndam, N.T.Milet, J.Basco, L.K.Aniweh, Y.Tahar, R.2022-04-272022-04-272022https://doi.org/10.1186/s12936-022-04139-0http://ugspace.ug.edu.gh/handle/123456789/38001Research ArticleBackground: Cytoadhesion and sequestration of Plasmodium falciparum infected red blood cells (iRBC) in the microvasculature of vital organs are a major cause of malaria pathology. Several studies have provided evidence on the implication of the human host intercellular adhesion molecule-1 (ICAM-1) as a major receptor for iRBCs binding to P. falciparum erythrocyte membrane protein 1 (PfEMP1) in the development of severe and cerebral malaria. The genetic polymorphism K29M in the immunoglobulin-like domain of ICAM-1, known as ICAM-1Kilifi, has been associated with either increased or decreased risk of developing cerebral malaria. Methods: To provide more conclusive results, the genetic polymorphism of ICAM-1Kilifi was assessed by PCR and sequencing in blood samples from 215 Beninese children who presented with either mild or severe malaria including cerebral malaria. Results and conclusions: The results showed that in this cohort of Beninese children, the ICAM-1kilifi variant is present at the frequencies of 0.27, similar to the frequency observed in other African countries. This ICAM-1kilifi variant was not associated with disease severity in agreement with other findings from the Gambia, Tanzania, Malawi, Gabon, and Thailand, suggesting no evidence of a direct link between this polymorphism and the pathogenesis of severe and cerebral malaria.enPlasmodium falciparumMalariacerebral malariaPolymorphismICAM-1ICAM-1kilifiArticle