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Metabolic Pathway Reconstruction for Malaria Parasite Plasmodium falciparum

Human malaria is caused by infection with four species of the intracellular parasitic protozoan genus Plasmodium that are transmitted by Anopheles mosquitoes. Of these four species, Plasmodium falciparum is the most lethal. At present, at least 300 million people are affected by malaria globally and accounts for 0.7-2.7 million annual deaths. The development of resistance in the parasite to antimalarial drugs, the lack of any licensed malaria vaccine and the fundamental complexity inherent in the malaria parasite, mean there is an urgent need to better understand the function of P. falciparum genes and their biological role to support the development of effective antimalarial strategies. P. falciparum genome indicates the presence of 5,432 genes spread across 14 chromosomes, a mitochondrial genome and a circular plastid genome. Notably, more than 60% are hypothetical proteins [1]. This fact emphasizes the need to elucidate gene function by somehow, new strategies. In this research, we focus on KEGG metabolic pathways [2] in P. falciparum. Currently, there are gaps in some paths in P. falciparum metabolic pathways partly because of the insufficient annotation. We try to resolve such missing enzymes by using the virtual enzyme (V-zyme) system [4] and KEGG ortholog clusters (OCs).