Davis, Morgan; Edvalson, Logan; Busath, David (Brigham Young University)
Faculty Advisor: Busath, David (Life Science, Physiology and Developmental Biology)
Influenza infection, and subsequent pneumonias, are the cause of over fifty thousand deaths in the United States per year, and, according to the CDC, influenza is the 8th leading cause of death in this country. Research into the pathogenesis of influenza elucidates critical interactions that take place during different phases of infection which can be targeted by novel drug therapies. Our lab has focused on discovering the role of of PDGFR and VEGFR and other Receptor Tyrosine Kinases (RTKs) in aiding viral infection. RTK activation is reported to be important for successful viral infection, and our project has focused on three different RTKs: VEGFR, PDGFR, and endothelial growth factor receptor (EGFR). In these experiments, Madin Darby Canine Kidney (MDCK) cells were bathed in growth medium containing a specific RTK inhibitor, and then infected with the influenza virus. The vitality of the cells was measured using crystal violet staining and spectrophotometer results. The data showed that using a drug called imatinib—a potent PDGFR inhibitor—resulted in the highest cellular vitality while VEGFR inhibitors developed here at BYU also showed anti-influenza activity. This suggests that the influenza virus is at least partially dependent on PDGFR and VEGFR activation to enhance its life cycle. Future experimentation will study which of the many branches of these receptor's phosphorylation cascades are being utilized by the virus.