Scientists have for years been puzzled by why drugs are sometimes effective in treating parasitic diseases, while other times they have little or no effect.
In research published in the Journal of Experimental Medicine, a team of scientists led by Boris Striepen at UGA provides both physiological and genetic explanations for the disparities.
Striepen and his team study Apicomplexa, a large group of parasitic microorganisms that includes the causative agents for malaria, cryptosporidiosis and toxoplasmosis, three important infectious diseases worldwide.
Most of these parasites have an apicoplast, a remnant chloroplast. Chloroplasts are the green cellular structures that plants and algae use to harvest the energy of sunlight.
Researchers in Striepen’s lab have been studying the apicoplast’s functions while trying to determine which are essential to parasite survival.
The study confirms that the ability of the apicoplast to produce certain lipids called isoprenoids is likely its most important function and a drug target in a broader group of pathogens than initially thought. It also points to potential mechanisms of future drug resistance in malaria, a mosquito-borne infectious disease that infects millions of people a year worldwide.
Striepen’s team demonstrated that the critical difference in the effectiveness of some drugs acting on the apicoplast lies in their uptake (or not) by the parasite. The antibiotic fosmidomycin is effective against malaria, but not against most other apicomplexan parasites, including Toxoplasma.
The scientists determined that the parasite plasma membrane is a critical barrier to drug uptake in some parasites.
