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In this paper, we consider the combined effects of cytotoxic T lymphocyte (CTL) responses on the competition dynamics of two Simian immunodeficiency virus (SIV) strains model. One of strains concerns a relatively slowly replicating and mildly cytopathic virus in the early infection (SIVMneCL8), the other is faster replicating and more cytopathic virus at later stages of the infection (SIVMne170). It is shown that the global dynamics of the ordinary differential equations can be determined by several threshold parameters, and we prove the global stability of the equilibria by rigorous mathematical analysis. To account for a series of infection mechanism leading to viral production, we incorporate time delays in the infection term. Using the methods of constructing suitable Lyapunov functionals and LaSalle’s invariance principle, we obtain the sufficient conditions for the global attractiveness of infection-free equilibrium with both virus strains going extinct, single-infection equilibrium with one of two virus strains out-competing the other one and the two strains coexisting infection equilibrium. We establish that the intracellular delays can destabilize the single-infection equilibrium leading to Hopf bifurcation and periodic oscillations. We show that introduction of immune responses is responsible for the coexistence of two virus strains and the intracellular delays may alter the two-strain competition results. Numerical simulations are presented to illustrate the theoretical conclusions. [ABSTRACT FROM AUTHOR]

The literature suggests that effective defence against tumour cells requires contributions from both Natural Killer (NK) cells and CD 8 + T cells. NK cells are spontaneously active against infected target cells, whereas CD 8 + T cells take some times to activate cell called as cell-specific targeting, to kill the virus. The interaction between NK cells and tumour cells has produced the other CD 8 + T cell, called tumour-specific CD 8 + T cells. We illustrate the tumour–immune interaction through mathematical modelling by considering the cell cycle. The interaction of the cells is described by a system of delay differential equations, and the delay, τ represent time taken for tumour cell reside interphase. The stability analysis and the bifurcation behaviour of the system are analysed. We established the stability of the model by analysing the characteristic equation to produce a stability region. The stability region is split into two regions, tumour decay and tumour growth. By applying the Routh–Hurwitz Criteria, the analysis of the trivial and interior equilibrium point of the model provides conditions for stability and is illustrated in the stability map. Numerical simulation is carried out to show oscillations through Hopf Bifurcation, and stability switching is found for the delay system. The result also showed that the interaction of NK cells with tumour cells could suppress tumour cells since it can increase the population of CD 8 + T cells. This concluded that the inclusion of delay and immune responses (NK-CD 8 + T cells) into consideration gives us a deep insight into the tumour growth and helps us understand how their interactions contribute to kill tumour cells. [ABSTRACT FROM AUTHOR]

This paper deals with stability and Hopf bifurcation analyses of a mathematical model of HIV infection of CD4+ T-cells. The model is based on a system of delay differential equations with logistic growth term and antiretroviral treatment with a discrete time delay, which plays a main role in changing the stability of each steady state. By fixing the time delay as a bifurcation parameter, we get a limit cycle bifurcation about the infected steady state. We study the effect of the time delay on the stability of the endemically infected equilibrium. We derive explicit formulae to determine the stability and direction of the limit cycles by using center manifold theory and normal form method. Numerical simulations are presented to illustrate the results. [ABSTRACT FROM AUTHOR]

We consider a four-dimensional HIV model that includes healthy cells, infected cells, primary cytotoxic T-lymphocyte response (CTLp), and secondary cytotoxic T-lymphocyte response (CTLe). The CTL memory generation depends on CD4+ T-cell help, and infection of CD4+ T cells results in impaired T-cell help. We show that the system has up to five equilibria. By the Routh–Hurwitz theorem and central manifold theorem we obtain some sufficient conditions for the local stability, globally stability of the equilibria, and the bifurcations. We still discover the bistability case where in the system there may coexist two stable equilibria or a stable equilibrium together with a stable limit cycle. Several numerical analyses are carried out to illustrate the validity of our theoretical results. [ABSTRACT FROM AUTHOR]