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Title: | Promoter Polymorphism of the Anion-Exchange Protein 1 Associated with Severe Malarial Anemia and Fatality |
Authors: | Agbenyega, Edward Tsiri Kalckreuth, Vera von Evans, Jennifer A. Timmann, Christian Kuhn, Daniela Horstmann, Rolf D. May, Ju¨rgen |
Issue Date: | 1-Feb-2006 |
Publisher: | Infectious Diseases Society of America |
Citation: | Infectious Diseases Society of America, 2006 |
Abstract: | The anion-exchange protein 1 (AE1 or band 3) is involved in the erythrocyte invasion of the malaria parasite
Plasmodium falciparum, the adhesion of infected erythrocytes to endothelial cells, and the regulation of acidbase
homeostasis, which is a critical factor for human survival in severe malaria. A variant of the AE1 gene
promoter 512 base pairs (bp) distant from the transcription start site and 5699 bp from the translation start
codon (AE1 5699TrC) has been shown to be highly frequent in a population from the Ashanti region, Ghana.
In a matched-pair case-control study (736 pairs), children heterozygous for the mutation (AE1 5699CT) had an
increased risk of severe malarial anemia (odds ratio [OR], 1.45 [95% confidenc interval {CI}, 1.05–2.01];
P ! .03). In children who developed this complication, carriers of the mutation AE1 5699C had a higher fatality
rate than those with the genotype AE1 5699TT (relative risk, 7.1 [95% CI, 1.0–52.8]). Moreover, in children with
cerebral malaria, AE1 5699C was positively associated with a distinctive metabolic acidosis (P ! .002), and results
of luciferase assays showed higher transcriptional activity of the AE1 5699C allele. These results demonstrate
that the AE1 promoter allele might influenc the infection phenotype and the risk of fatal outcome in children
with severe malaria. In this regard, a crucial role of the AE1 protein in malaria is emphasized. |
Description: | This article is published at Infectious Diseases Society of America |
URI: | http://hdl.handle.net/123456789/15683 |
Appears in Collections: | College of Health Sciences
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