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Background  Two recent reports have identified the Endothelial Protein C Receptor (EPCR) as a key molecule implicated in severe malaria pathology. First, it was shown that EPCR in the human microvasculature mediates sequestration of  Plasmodium falciparum -infected erythrocytes. Second, microvascular thrombosis, one of the major processes causing cerebral malaria, was linked to a reduction in EPCR expression in cerebral endothelial layers. It was speculated that genetic variation affecting EPCR functionality could influence susceptibility to severe malaria phenotypes, rendering  PROCR , the gene encoding EPCR, a promising candidate for an association study.    Methods  Here, we performed an association study including high-resolution variant discovery of rare and frequent genetic variants in the  PROCR  gene. The study group, which previously has proven to be a valuable tool for studying the genetics of malaria, comprised 1,905 severe malaria cases aged 1–156 months and 1,866 apparently healthy children aged 2–161 months from the Ashanti Region in Ghana, West Africa, where malaria is highly endemic. Association of genetic variation with severe malaria phenotypes was examined on the basis of single variants, reconstructed haplotypes, and rare variant analyses.    Results  A total of 41 genetic variants were detected in regulatory and coding regions of  PROCR , 17 of which were previously unknown genetic variants. In association tests, none of the single variants, haplotypes or rare variants showed evidence for an association with severe malaria, cerebral malaria, or severe malaria anemia.    Conclusion  Here we present the first analysis of genetic variation in the  PROCR  gene in the context of severe malaria in African subjects and show that genetic variation in the  PROCR  gene in our study population does not influence susceptibility to major severe malaria phenotypes.

Endothelial Protein C Receptor Gene Variants Not Associated with Severe Malaria in Ghanaian Children