Monica High
National Institute of Environmental Health Sciences
111 TW Alexander Drive
Research Triangle Park, NC 27709
Tel: (919) 316-4673
Fax: (919) 541-4133
Education
Doctorate of Philosophy
Curriculum in Toxicology
Research Advisor: Steven Kleeberger
Date of Matriculation: 2004
Bachelor of Science in Biology
Florida A&M University, Tallahassee, FL, 2004
Awards
2006 Minority Trainee Research Forum National Abstract Competition, Cx3cr1 contributes to ozone-induced pulmonary inflammation in the mouse, Miami, FL
2007 American Thoracic Society Minority Travel Award, San Francisco, CA
Dissertation
“Positional cloning of RSV susceptibility in inbred mice”
Advisor: Steven Kleeberger
2008 American Thoracic Society abstract submission
Purpose: Respiratory Syncytial Virus (RSV) is the leading cause of lower respiratory tract infection (LRTI) in infants. Approximately 70% of infants are infected with RSV within the first year of life. Epidemiological studies show that individuals have varying responses to RSV infection, ranging from “cold-like” symptoms to death. Previous in vivo studies have suggested that RSV susceptibility is a polygenic trait; however, the specific genes regulating this phenotype have yet to be identified. The purpose of this research is to identify the genetic polymorphisms that contribute to RSV susceptibility.
Methods: Inbred mouse strains were infected with a single dose of 1x106 plaque forming units (pfu) of RSV or control and sacrificed after 1 and 5 days post-infection (pi). Bronchoalveolar lavage fluid (BALF) was collected at the time of necropsy and analyzed for total protein (marker of lung permeability) and total cells. Lungs from each strain were collected and used for pathology analysis.
Results: No significant differences in mean numbers of BALF inflammatory cells, total protein, and lung pathology were found between strains infected with control. The inbred strains used in this study demonstrated an apparent strain distribution pattern in response to RSV infection, in which C3H/HeJ is the most resistant strain, and BALB/cJ is the most susceptible strain. There is a 4.5-fold difference between the most resistant and most susceptible strains.
Conclusions: Inflammatory, lung permeability and pathology data from this study indicate that different strains of inbred mice respond differently to RSV. The observed strain distribution pattern confirms that RSV susceptibility has a genetic component