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Abstract

Background: Sub-Saharan African countries are plagued by an adaptable parasite, Trypanosoma brucei, T.b., with a very high iron dependency. This protozoan parasite is the causative agent for Human African Trypanosomiasis (HAT), otherwise known as sleeping sickness. Two specific subspecies of interest include T.b. gambiense and T. b. rhodesiense. They lead to either a chronic or acute form of the fatal sleeping sickness disease, respectively. Few effective methods of treatment are available. The goal of this research project is to propose pharmaceutical drug target(s) to combat T. brucei infections. Methods: Studies analyzed the reaction pathways that take place during the parasite’s life cycle, identified the natural and chemically produced superoxide radicals within the parasite, and also elucidated the differences in the parasite’s life processes will allow for the derivation of a plausible methods to cease the infection cycle of the T. brucei parasite. The impact of these factors on preventing or reducing the virulence of the infection by T. brucei was assessed using computer-aided simulation software named CLEMS, Command-Line Electro-Metabolomics Software. We monitored the concentrations of oxygen, glucose and dihydroxyacetone phosphate, DHAP, given their importance for the survival of the parasite. Oxygen concentration peaked soon after the start of the simulation before achieving steady state with a concentration comparable to that of the mammalian environment simulated; glucose concentration was constant throughout the simulation again consistent with the environment where the parasite is evolving; finally, results showed a decrease in DHAP concentration followed by steady state. Any process, which contributes to further decreasing DHAP concentration, is likely to be detrimental to the T. brucei. Other processes, such as superoxide radical degradation, will be considered in concert to the ones assessed in this study to develop suitable drug targets.

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