Internships

Fatu S. Conteh ’10

It’s a fact: malaria kills over a million people a year and stands in the way of economic development for many countries where the disease is endemic. Past efforts to eradicate this deadly disease with drug treatments like quinine, chloriquine, and other antimalarials have proven futile as the malaria parasite (Plasmodium Falciparum) has developed resistance to these drugs. However, artemisinin, with no known stable resistance, has been ganarring momentous support from both the non-profit and for-profit sectors as the first line drug treatment for uncomplicated and multi-drug resistant P. Falciparum malaria.

Currently, according to the World Health Organization, since 2001, a total of 56 countries have adopted one of the WHO recommended artemisinin-based combination therapies, several as first-line treatment and a few as second-line. With this increasing use of Artemisinin comes the threat of the malaria parasite developing resistance to the drug. There is a growing concern in the field of malaria therapy that if or when the parasite develops resistance to artemisinin, like it has done with other antimalarials, no one will know how to combat the resistance because the mechanism of action of artemisinin is uncertain.

There are two strong competing hypothesis as to how the drug actually kills the parasite. One hypothesis, the multiple targets hypothesis, contends that artemisinin kills the parasite by reacting with the iron in hemin to produce oxygen radicals. The other hypothesis argues that artemisinin acts via a specific protein. My research this past summer was focused on using novel protocols in proteomics to find the protein target(s) of artemisnin, with hopes of disproving one of these two hypothesis. The results I obtained from my protein gels at the end were inconclusive and further experiments are needed to clarify my data.