HOUSTON, Oct. 13, 2011 Malaria has been one of the world's biggest killers for as long as records have been kept. With resistance to existing antimalarial drugs on the rise, there is a renewed push to find different ways to fight it. Two University of Houston (UH) engineers have stepped up to the plate to answer the call.
Jeffery Rimer and Peter Vekilov, both with the department of chemical and biomolecular engineering, recently were awarded a grant from the U.S. Department of Defense (DOD) to create an entirely new platform for developing antimalarial drugs. Like existing antimalarial drugs, this new platform will target plasmodium, which is the parasite that causes malaria, by utilizing a quirk in the infection process.
Typically introduced into hosts through a mosquito bite, plasmodium enters a host's red blood cells where it consumes the hemoglobin by breaking it down. However, one subunit of hemoglobin the parasite cannot use is heme, which is the part of the blood that helps transport oxygen to the other parts of the body. Left alone, heme is highly toxic toxic enough, in fact, to kill the parasite and prevent an infection from taking hold.
Unfortunately, as the parasite has evolved, it segregates the heme into little crystals. If the heme is sequestered in crystals, it can't kill the parasite. Existing antimalarial medications presumably work by preventing the formation and growth of heme crystals. As a result, heme molecules released by hemoglobin consumption usually are able to kill the parasite. However, the effectiveness of these drugs has begun to wane.
Since the precise nature of how these drugs prevent crystal formation is unknown, Vekilov and Rimer will work to uncover the process of heme crystal formation and then determine what kind of molecules could inhibit crystallization. Vekilov believes that heme molecules attach to crystals at kinks that are sites on the crystal surface favorable for the addi
|Contact: Lisa Merkl|
University of Houston