Georgia Institute of Technology College of Sciences

Mathematical modeling of viruses, such as HIV, has been an extensive area of research over the past two decades. For HIV, some important factors that affect within-host dynamics include: the CTL (Cytotoxic T Lymphocyte) immune response, intra-host diversity, and heterogeneities of the infected cell lifecycle. Motivated by these factors, I consider several extensions of a standard virus model. First, I analyze a cell infection-age structured PDE model with multiple virus strains. The main result is that the single-strain equilibrium corresponding to the virus strain with maximal reproduction number is a global attractor, i.e. competitive exclusion occurs. Next, I investigate the effect of CTL immune response acting at different times in the infected-cell lifecycle based on recent studies demonstrating superior viral clearance efficacy of certain CTL clones that recognize infected cells early in their lifecycle. Interestingly, explicit inclusion of early recognition CTLs can induce oscillatory dynamics and promote coexistence of multiple distinct CTL populations. Finally, I discuss several directions of ongoing modeling work attempting to capture complex HIV-immune system interactions suggested by experimental data.