Abstract:

 Models using DDEs are more consistent with the biology and provide different estimates for certain kinetic parameters. We will show the differences we have found when comparing these models to existing patient data. We then will discuss properties of these models that exhibit Hopf bifurcations when examining primary infection and show how the model predicts the somewhat random nature of early pathogenesis. Finally, I will present a new model that allows for a varying death rate and production rate due to the age of cellular infection and discuss its implications for modeling HIV-1.