Research

Host-pathogen interactions in Plasmodium falciparum

The symptoms associated with malaria are directly linked to infection of red blood cells, and their extensive remodeling by the parasite.  The parasite exports proteins that interact with the red blood cell cytoskeleton or become inserted into the red cell membrane.  These induce stiffening of infected cells and increase their propensity to engage in new cell-cell interactions.  These properties underlie parasite sequestration within the microvasculature of vital organs, such as the brain and lungs.  This ultimately contributes to potentially fatal severe malaria outcomes, such as cerebral malaria.

We are interested in better understanding the pathophysiology of severe malarial disease.  Specifically, we seek further insight into how organ-specific distribution and burden of parasites interact to influence the likelihood of a severe malaria outcome, and whether dysfunction of a specific organ system correlates with these parameters.  To address these questions, we are developing molecular probes to facilitate dynamic and quantitative molecular imaging of genetically unmodified parasites in the native host.  Simultaneously, we are also interested in developing these reagents as diagnostic tools and potential therapeutics.