“Our primary aim is to identify the genes that underlie drug resistance in the malaria parasite (Plasmodium falciparum) and the parasitic fluke, Schistosoma mansoni. Identification of these genes will allow us to monitor resistance spread in the field, to redesign drugs to restore efficacy, and to better understand the dynamics of resistance evolution. ”
Parasitic diseases still plague broad swathes of the world’s developing countries, reducing childhood survival rates and stunting economic growth. However, genome sequence data for the pathogens involved and funding from organizations such as the Bill and Melinda Gates Foundation have generated new hope of controlling or even eliminating these diseases. Our laboratory focuses on two of the most important human parasites – malaria, caused by the protozoan Plasmodium falciparum and Schistosomiasis, caused by the blood fluke in the genus Schistosoma.
Malaria infects around 500 million people each year, killing 1.7-2.5 million people. There is currently no vaccine and resistance to all five classes of antimalarial drugs has now been reported. We are using three different strategies to identify genes that underlie resistance. First, we are using genome-wide association methods to systematically search for the genes involved. As the malaria genome is relatively small, we can use whole genome sequence information from populations of parasites to achieve this goal. Second, we are examining the role of copy number variation – already this approach has characterized an important gene involved in drug resistance. Finally, we are selecting resistant parasites in the laboratory and using next generation sequencing methods to identify the genetic changes that have occurred. Our work involves collaborators in South America, Africa, and Southeast Asia.
Schistosomiasis - otherwise known as Bilharzia – is caused by blood flukes (Schistosoma spp.). These parasites infect over 270 million people in Africa, South America and Asia, and utilize snail intermediate hosts. The adult worms live in the blood vessels, but the eggs cause pathology by lodging in the liver or intestine wall, where granulomas form resulting in periportal fibrosis and hepatosplenic disease. Our work with schistosomes uses a different approach to genetic mapping. We have conducted genetic crosses in the laboratory to generate the first genetic map for a human helminth parasite. This allowed us to assign most of the fragmented genome sequence to individual chromosomes. We are now exploiting this map and using linkage mapping methods to identify genes that underlie oxamniquine and praziquantel resistance. Our schistosome research involves collaborators in San Antonio (Health Science Center), Italy and the UK.
Lab members Shalini Nair (Sr Research Associate) Daniel Sudimack (Research Assistant)
Departed Charles D. Criscione (Postdoctoral Scientist). Now an Assistant Professor at Texas A&M University.
Joel Anderson (Research Associate). Now a Natural Resource Specialist working on genetics of marine organisms with Texas Parks and Wildlife.
Denae Nash (undegraduate intern). Now a Doctoral student in Cell and Molecular Biology at Baylor University.
Cherise Rohr (Postdoctoral scientist). Now a Research Molecular Biologist working on ticks and Babesia at the USDA-ARS U.S. Livestock Insects Research Laboratory in Kerrville, Texas.
