Research & Funding

Raegan Petch, University of Pennsylvania
Mentor: Paul F. Bates, PhD, Professor of Microbiology, Department of Microbiology, University of Pennsylvania

Project Overview: I am working to develop a second-generation recombinant vesicular stomatitis virus vaccine for Severe Fever with Thrombocytopenia Syndrome Virus (rVSV-SFTSV). First generation vaccines are highly attenuated in cell culture, which makes it difficult to produce sufficient vaccine for clinical trials. I am introducing mutations to the glycoprotein of SFTSV that we hypothesize will increase the replication capacity of the virus in vitro and in vivo and improve the immunogenicity of the vaccine candidate in animal models.

Daana Roach, University of Pennsylvania
Mentor: Kathryn Hamilton, PhD, Assistant Professor of Pediatrics (Gastroenterology, Hepatology and Nutrition), Children’s Hospital of Philadelphia, University of Philadelphia

Project Overview: Lipocalin-2 (LCN2), initially identified as a neutrophilic protein for innate immunity, has broader roles. Our lab found LCN2 expression in the intestinal epithelium of inflammatory bowel disease (IBD) patients, not in healthy subjects. The impact of epithelial-specific LCN2 on function and physiology is less understood. Goblet cells, a secretory cell type in the intestinal epithelium, express LCN2 and secrete mucus, including antimicrobial peptides like LCN2, affecting the epithelium-luminal contents interaction. LCN2 also influences immune cell activity. In IBD, chronic inflammation occurs due to persistent intestinal epithelium injury and repeated exposure of mucosal immune cells to luminal contents. The effect of epithelial-specific LCN2 on immune cell activity in IBD and at homeostasis is unclear. The project aims to understand how goblet-cell expression of LCN2 influences cell function in IBD and epithelial-immune interaction.

Helen Stillwell, University of Pennsylvania
Mentor: Susan R. Weiss, PhD, Professor and Vice Chair, Department of Microbiology, University of Pennsylvania

Project Overview: In 2012, wild-type MERS-CoV spilled over from camels into humans in Saudi Arabia, causing severe lower respiratory tract disease with a mortality rate of 36%. In northern Africa, related clade C MERS viruses circulate in camels, but to not appear to cause disease in humans. Helen is studying the differences in the innate immune response to these viruses in human and camelid primary nasal epithelial air-liquid interface (ALI) cultures to better understand this divergence in pathogenicity.