| Description |
We develop mathematical models to study the effect of changes to the regulation of cell division during human papillomavirus (HPV) infections at the molecular and the tissue level. At the molecular level, the HPV viral protein E7 binds to and inactivates the retinoblastoma tumor suppressor protein (RB), a key regulatory protein of the cell cycle. We examine how the regulation of the G1/S transition is modified due to growth factor concentration, E7 concentration, and differences in RB binding affinity. At the tissue level, HPV infected cells interact with uninfected cells during the viral life cycle, which may influence disease progression. We develop a mathematical model of homeostatic tissue that incorporates cell division due to growth factor and low cell density, and cell delamination due to high cell density, which we use as a framework to study how growth factor, growth factor receptors, and cell density contribute to the rate and spread of HPV infections in tissue. |
