Bifurcation and stability analysis of within host HIV dynamics with multiple infections and intracellular delay.

Abstract

Human immunodeficiency virus (HIV) manifests multiple infections in CD4+ T cells, by binding its envelope proteins to CD4 receptors. Understanding these biological processes is crucial for effective interventions against HIV/AIDS. Here, we propose a mathematical model that accounts for the multiple infections of CD4+ T cells and an intracellular delay in the dynamics of HIV infection. We study the model system and establish the conditions under which the disease-free equilibrium point and the endemic equilibrium point are locally and globally asymptotically stable. We further provide the conditions under which these equilibrium points undergo forward or backward transcritical bifurcations for the autonomous model and Hopf bifurcation for both the delay model and autonomous models. Our simulation results show that an increase in the rate of multiple infections of CD4+ T cells stabilizes the endemic equilibrium point through Hopf bifurcation. However, in the presence of an intracellular delay, the model system evinces three types of stability scenarios at the endemic equilibrium point-instability switch, stability switch, and stability invariance and is demonstrated using bi-parameter diagrams. One of the novel aspects of this study is exhibiting all these interesting nonlinear dynamical results within a single model incorporating a single time delay.