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Elizabeth Egan, MD, PhD is an Assistant Professor in the Division of Infectious Diseases in the Department of Pediatrics. She obtained her B.A. at Barnard College in NYC and her MD/PhD from Tufts University School of Medicine in Boston. Prior to medical school she worked in Will Talbot's lab studying early pattern formation in zebrafish. Her PhD in Matthew Waldor's lab focused on defining essential replication factors for the two Vibrio cholerae chromosomes. As a postdoc in Manoj Duraisingh's lab at Harvard School of Public Health she performed a genetic screen to identify critical host factors for Plasmodium falciparum malaria using red blood cells derived from hematopoietic stem cells. Clinically, she completed training in Pediatrics and Pediatric Infectious Diseases at Boston Children's Hospital and now sees patients on the Pediatric Infectious Diseases service at Lucille Packard Children's Hospital. Her research is focused on understanding how host factors from the human erythrocyte influence the biology and pathogenesis of the malaria parasite Plasmodium falciparum.
Severe malaria caused by Plasmodium falciparum is a leading cause of morbidity and mortality in the developing world, particularly among young children and pregnant women. Population genetic studies dating back to the mid-20th century first proposed that erythrocytes (red blood cells), the host cell for P. falciparum, have been under natural selection due to malaria. Hemoglobinopathies, thalassemias, ovalocytosis, and G6PD deficiency are all examples of red cell disorders that appear to provide protection against severe malaria. <br/><br/>Although the notion that malaria has helped shape the human genome is well- accepted, the lack of a nucleus in human erythrocytes has hindered our ability to study genetic interactions between these unusual host cells and P. falciparum parasites. Recently, we developed a hematopoietic stem cell-based approach to tackle this issue, in which we can genetically alter nucleated hematopoietic precursor cells and differentiate them ex-vivo to mature erythrocytes that can be infected by P. falciparum. Using this approach, we performed a forward genetic screen of human blood groups to identify critical host factors for P. falciparum, and discovered several candidates that appear to be required for efficient parasite invasion of red blood cells. We found that the Cromer blood group antigen CD55 (DAF) is essential for parasite invasion and is necessary for proper attachment of merozoites to the erythrocyte surface. Importantly the requirement for CD55 appears to be strain-transcendent, suggesting that it may act as a critical receptor during malaria infection. <br/><br/>We are currently pursuing fundamental questions related to host-pathogen interactions in malaria, with the host erythrocyte as a focal point. We employ a variety of approaches spanning molecular parasitology, stem cell biology, cell biology, biochemistry and genomics. We welcome self-motivated individuals interested in joining us as we seek to learn more about the fascinating biology underlying host-pathogen interactions in malaria.