Document Type

Poster

Publication Date

Spring 2014

Abstract

In sub-Saharan Africa the protozoan parasite, Trypanosoma brucei, continues to be of major concern for the health and economic development of the region. This parasite is known to cause human African trypanosomiasis (HAT or African sleeping sickness) and nagana in livestock such as cattle. Social behaviors, such as colonization and migration, are important in the study of T. brucei because of the way the parasite infects its mammalian host. During the fly bloodmeal, the parasite first passes into the gut but then eventually migrates to the fly salivary glands where it will continue to develop before transmission as a parasitic form able to infect and cause disease in humans and livestock. Past research has shown that the social motility, the ability of the multitude of parasites in an infection to move in a coordinated fashion, is affected by the removal of the T. brucei hexokinase 2 (TbHK2) gene or expression of excess copies of the TbHK2 protein. In exploring social motility phenotypes of TbHK2-deficient insect stage (procylic form, PF)T. brucei parasites and parental forms complemented with excess TbHK2 gene, this project aims to understand more about the role of TbHK2 in social motility of T. brucei. Additionally, in order to understand how hexokinase 2 could be targeted by enzyme inhibitors, known hexokinase 1 inhibitors are explored for their effects on TbHK2 complemented cells compared to the parental strain parasites.

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