The invasion of erythrocytes by Plasmodium falciparum parasites produces aninfection that causes major changes in the structure, composition, antigenicity and function of the host cell membrane. During infection, the parasite actively imports obligate nutrients from the serum and exports lipids, proteins and membranes to the erythrocyte cytoplasm and the erythrocyte membrane. The regulation of these pathways must be underparasite control since mature erythrocytes have limited lipid synthetic or metabolic capabilities and do not have the machinery to synthesize or process proteins. Elucidation of trafficking pathways is complex in Plasmodia-infected erythrocytes compared to other eukaryotic cells, since the parasite is separated from the serum by its plasma membrane, the parasitophorous vacuolar membrane PVM and the erythrocyte membrane. There remains a long-felt need to identify the cellular components of these trafficking pathways to gain a better understanding of transport mechanisms in malaria-infected erythrocytes.

The laboratory is engaged in three areas of inquiry:

1. Elucidation of parasite protein trafficking pathways from intracellular parasites to the erythrocyte cytosol and host cell membrane.
2. Determination of the mechanism of hemoglobin uptake and transport by intraerythrocytic parasites
3. Characterization of parasite DNA repair pathways (e.g. base excision and mismatch repair). Continued identification of the cellular components of these trafficking pathways to gain a better understanding of transport mechanisms in malaria-infected erythrocytes.

PhD, Chemistry, Rutgers University (1980)