Malaria is caused by infection with mosquito-borne protozoan Plasmodium parasites. It remains a formidable global health problem, with over two hundred million cases each year and between half a million deaths, and a large contributor to childhood and maternal morbidity and mortality in large regions of the world. With increasing drug-resistance and no vaccine, a potential public health disaster looms.
Plasmodium spp. are obligatory intracellular parasites, with a life-cycle of switching between insect vectors and vertebrate hosts. They are not model organisms, and we still have limited insight into the fundamental biology of these parasites. Our research program focuses on identifying the molecular determinants of infection and pathogenesis caused by the most virulent of the human malaria parasites Plasmodium falciparum. We focus on the blood-stage of infection, which is relevant both to clinical disease and transmission to mosquitoes. We are developing and applying state-of-the-art genetic methodologies, combined with cell biology and genomic approaches, to study critical parasite and host determinants required for proliferation. Our approaches permit both an analysis of gene function and their validation as targets for the development of novel drugs and vaccines.
Research in our laboratory has focused on understanding the biology of malaria parasites and their interactions with their host red blood cells in the following areas:
1. Molecular analysis of Plasmodium invasion of red blood cells: ligand-receptor interactions and signal transduction.
2. Red blood cell determinants of malaria infection: invasion, growth and sexual development.
3. Epigenetic regulation of virulence gene expression and sexual development in malaria parasites.
4. Molecular barriers to the zoonotic transmission of malaria.
5. Engineering in vitro culture and genetic systems for Plasmodium spp. and Babesia spp.
6. Field studies with parasite isolates in India (Goa) and Senegal (Dakar).