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In this paper, the dynamical behaviors of a multiple delayed HIV-1 infection model which describes the interactions of humoral, cytotoxic T lymphocyte (CTL) immune responses, and two modes of transmission that are the classical virus-to-cell infection and the direct cell-to-cell transmission are investigated. The model incorporates three delays, including the delays of cell infection, virus production and activation of immune response. We first prove the well-posedness of the model, and calculate the biological existence of equilibria and the reproduction numbers, which contain virus infection, humoral immune response, CTL immune response, CTL immune competition, and humoral immune competition. Further, the threshold conditions for the local and global stability of the equilibria for infection-free, immune-free, antibody response, CTL response, and interior are established by utilizing linearization method and the Lyapunov functionals. The existence of Hopf bifurcation with immune delay as a bifurcation parameter is investigated by using the bifurcation theory. Numerical simulations are carried out to illustrate the theoretical results and reveal the effects of some key parameters on viral dynamics. [ABSTRACT FROM AUTHOR]

In this paper, the authors consider a four-compartmental HIV epidemiological model, which describes the interaction between HIV virus and two target cells, CD4 T cells and macrophages in vivo. It is proved that the bilinear incidence can cause the backward bifurcation, where a locally asymptotically stable disease-free equilibrium co-exists with a locally asymptotically stable endemic equilibrium when the basic reproduction number (R0) is less than unity. It is shown that a sequence of Hopf bifurcations occur at the endemic equilibrium by choosing one parameter of the model as the bifurcation parameter. Meanwhile, the global asymptotic stabilities of the equilibria are established by constructing suitable Lyapunov functions under some conditions. Furthermore, the authors develop an extended model by incorporating with the intracellular delays and derive global asymptotic stability of the delayed model by constructing Lyapunov functions. Some numerical simulations for justifying the theoretical analysis results are also given. [ABSTRACT FROM AUTHOR]

Abstract: In this paper, we study the dynamics of a mathematical model on primary and secondary cytotoxic T-lymphocyte (CTL) response to viral infections by Wodarz et al. This model has three equilibria and their stability criteria are discussed. The system transitions from one equilibrium to the next as the basic reproductive number, , increases. When increases even further, we analytically show that periodic solutions may arise from the third equilibrium via Hopf bifurcation. Numerical simulations of the model agree with the theoretical results and these dynamics occur within biologically realistic parameter range. The normal form theory is also applied to find the amplitude, phase and stability information on the limit cycles. Biological implications of the results are discussed. [Copyright &y& Elsevier]

We consider a Human Immunodeficiency Virus (HIV) model with a logistic growth term and continue the analysis of the previous article. We now take the viral diffusion in a two-dimensional environment. The model consists of two ODEs for the concentrations of the target T cells, the infected cells, and a parabolic PDE for the virus particles. We study the stability of the uninfected and infected equilibria, the occurrence of Hopf bifurcation and the stability of the periodic solutions. [ABSTRACT FROM AUTHOR]

Stable periodic oscillations have been shown to exist in mathematical models for the CTL response to HTLV-I infection. These periodic oscillations can be the result of mitosis of infected target CD4 cells, of a general form of response function, or of time delays in the CTL response. In this study, we show through a simple mathematical model that time delays in the CTL response process to HTLV-I infection can lead to the coexistence of multiple stable periodic solutions, which differ in amplitude and period, with their own basins of attraction. Our results imply that the dynamic interactions between the CTL immune response and HTLV-I infection are very complex, and that multi-stability in CTL response dynamics can exist in the form of coexisting stable oscillations instead of stable equilibria. Biologically, our findings imply that different routes or initial dosages of the viral infection may lead to quantitatively and qualitatively different outcomes. [ABSTRACT FROM AUTHOR]