Within-host dynamics of HIV/AIDS




Xie, Xinqi

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This thesis first investigates within-host HIV models for the acute stage. These models incorporate the immune responses and helper T cells produced from the activation of naive CD4 T cells. Because both naive CD4 T cells and helper T cells are susceptible classes, backward bifurcation and bistability may occur. We start with a simple model that ignores the CD8 T cell dynamics, then extend it to include this dynamics. We also extend our model to consider the latent infection of naive CD4 T cells. Backward bifurcation occurs in all these models. We numerically investigate the stability of viral equilibria, and show the bistability caused by backward bifurcation. Increasing the inflow of CTLs prevents the backward bifurcation. With a large homeostatic source of healthy naive CD4 T cells, the disease is easier to establish when the basic reproduction number is less than one. Reducing the reproduction number below one is not sufficient to control the infection of HIV. Secondly, this thesis investigates the development of AIDS caused by viral diversity, as proposed by Wodarz et al. using a model that does not include the details of immune responses. We extend their model to include density dependence, and show that the viral load increases with viral diversity. To study if this result still holds with more realistic HIV dynamics, we incorporate viral diversity into our first model. We conclude theoretically that the total viral load is positively correlated with the number of viral strains, and viral diversity can drive the development of AIDS. We also find that the total CD4 T cell count does not always decrease with viral diversity. Thus further investigation is needed to fully understand the development of AIDS.



HIV, Within-host dynamics, Backward bifurcation