|Figure 1. Confocal image of HAE infected with RSV - the virus infected cells are green and the cilia are stained red (uninfected cells are not visualized).|
|Figure 2. H&E stained sections of HAE uninfected, or infected for the times indicated (2/4 days post inoculation). RSV infected cells are indicated by black arrows and infected cells shedding from the epithelium are evident by 4dpi|
My work focuses respiratory viral pathogen interactions with the lung epithelium. I am specifically interested in respiratory syncytial virus (RSV) and parainfluenza virus 3 (PIV3), viruses that commonly cause respiratory illness in infants, children, and individuals with underlying chronic lung disease. These viruses infect ciliated cells of the airway and my research focuses on viral control of apoptosis and shedding of the infected cell. We have identified the non-structural proteins NS1 and NS2 of RSV as having an integral role in shedding in an RSV infected cell. Current work is focused on identifying the mechanisms of innate immune control by NS1 and NS2 and the role of these proteins in delaying apoptosis and shedding of the infected ciliated cell. The long term goal of my project is to understand the physiological consequences of ciliated cell shedding during viral infection.
Contact Information7021 Thurston-Bowles Bldg.
The University of North Carolina at Chapel Hill
Campus Box #7248
Chapel Hill, NC 27599
Phone: (919) 966-7044
Fax: (919) 966-5178