Our research activities have been devoted to understanding the mechanisms by which this obligate intracellular parasite is able to survive within host cells and cause disease. We use a variety of molecular biology, cell biology and genetic techniques to understand the pathogenesis of toxoplasmosis. Molecular basis of T. gondii latency.
Most clinical toxoplasmosis is due to reactivation of the latent bradyzoite form.
We are using a molecular genetic approach to determine the mechanism by which T. gondii parasites switch from the tachyzoite form to the latent bradyzoite form. This differentiation is stress-induced, and our recent experiments implicate cyclic nucleotide signaling in bradyzoite formation. We are now clarifying the role of protein kinase A and other signaling molecules. Role of proteinases in invasion. T.gondii is an obligate intracellular parasite that must invade host cells in order to survive.