In its natural state, the malaria parasite, Plasmodium falciparum, leads a complicated life. It proceeds through a series of distinct developmental stages both in humans and in mosquitoes, the main vector for disease transmission. Malaria researchers typically circumvent this complexity by studying the parasite in cultured cells. Yet in this artificial setting, few differences have been found in the genes that are turned on or off in various strains of P. falciparum. That uniformity is surprising, because it fails to explain the drastically different courses experienced by malaria patients.
To explore the basis for these differences, first author Johanna Daily, an infectious disease physician at Brigham and Women's Hospital, assistant professor of medicine at Harvard Medical School, and a researcher at both the Harvard School of Public Health and the Broad Institute, set out to observe P. falciparum in its natural environment: the human circulation. Using small samples of blood collected from more than 40 malaria patients in Senegal, Daily and her colleagues worked meticulously to devise a method for isolating genetic material from parasites, allowing them to determine which of the nearly 6,000 P. falciparum genes are switched on or off during infection in humans. Importantly, all of the patients involved in the study harbored similar-looking parasites, yet their symptoms varied widely.
These clinical research efforts were led by Professor Souleymane Mboup and Dr. Daouda Ndiaye at Cheikh Anta Diop University. "This project would not have been possible without the dedicated work of our collaborators in Senegal," said co-author Dyann Wirth, a professor and chairman of the department of immunology and infectious diseases at the Harvard School of Public Health and the co-director of the Broad Institute'
|Contact: Nicole Davis|
Broad Institute of MIT and Harvard