Asymptotic properties of a HIV-1 infection model with time delay

Based on some important biological meanings, a class of more general HIV-1 infection models with time delay is proposed in the paper. In the HIV-1 infection model, time delay is used to describe the time between infection of uninfected target cells and the emission of viral particles on a cellular level as proposed by Herz et al. [A.V.M. Herz, S. Bonhoeffer, R.M. Anderson, R.M. May, M.A. Nowak, Viral dynamics in vivo: Limitations on estimates of intracellular delay and virus decay, Proc. Natl. Acad. Sci. USA 93 (1996) 7247-7251]. Then, the effect of time delay on stability of the equilibria of the HIV-1 infection model has been studied and sufficient criteria for local asymptotic stability of the infected equilibrium and global asymptotic stability of the viral free equilibrium are given.     

Global stability of an HIV-1 infection model with saturation infection and intracellular delay

In this paper, an HIV-1 infection model with a saturation infection rate and an intracellular delay accounting for the time between viral entry into a target cell and the production of new virus particles is investigated. By analyzing the characteristic equations, the local stability of an infection-free equilibrium and a chronic-infection equilibrium of the model is established. By using suitable Lyapunov functionals and the LaSalle invariant principle, it is proved that if the basic reproduction ratio is less than unity, the infection-free equilibrium is globally asymptotically stable; if the basic reproduction ratio is greater than unity, the chronic-infection equilibrium is globally asymptotically stable.     

The global dynamics of a model about HIV-1 infection in vivo

A four dimension ODE model is built to study the infection of human immunodeficiency virus (HIV) in vivo. We include in this model four components: the healthy T cells, the latent-infected T cells, the active-infected T cells and the HIV virus. Two types of HIV transmissions in vivo are also included in the model: the virus-to-cell transmission, and the cell-to-cell HIV transmission. There are two possible equilibriums: the healthy equilibrium, and the infected steady state. The basic reproduction number R ₀ is introduced. When R ₀ < 1, the healthy equilibrium is globally stable and when R ₀ > 1, the infected equilibrium exists and is globally stable. Through simulations, we find that, the cell-to-cell HIV transmission is very important for the final outcome of the HIV attacking. Some important clinical observations about the HIV infection situation in lymph node are also verified.      

Analysis of a mathematical predator-prey model with delay

We study the behavior of dynamic processes in a mathematical predator-prey model and show that the dynamical system may have a periodic solution whose period coincides with the delay. By the bifurcation method for stability analysis of periodic solutions, we establish that this periodic solution is unstable.     

Pseudo almost periodic dynamics of delay Nicholson's blowflies model with a linear harvesting term

In this paper, we investigate a class of delay Nicholson's blowflies model with a linear harvesting term, new criteria for the existence and convergence dynamics of positive pseudo almost periodic solutions are established by using the fixed point method and the properties of pseudo almost periodic function, together with constructing suitable Lyapunov functionals. The obtained results extend previously known results, and they also partially answer an open problem proposed by L. Berezansky et al. Finally, an example with simulation is presented to demonstrate the effectiveness of theoretical results. Copyright © 2014 John Wiley & Sons, Ltd.     

Long term dynamics of a reaction-diffusion system

We study a reaction-diffusion system of two parabolic differential equations describing the behavior of a nuclear reactor. We provide existence results for nontrivial periodic solutions, nonexistence results for stationary solutions and we prove that, depending on the value of the parameters, either the system admits a compact global attractor, or the solutions are unbounded.     

On the modeling of long-term HIV-1 infection dynamics

In this paper, we propose and study models of long-term Human Immunodeficiency Virus (HIV-1) infection. Our aim is to identify model mechanisms that allow one to explain the trends observed in clinical measurements of the number of CD4+ T-cells and virus throughout the long-term HIV-1 infection, from the acute phase until the onset of AIDS. To achieve our goal, we apply some standard methods of modeling and analysis of dynamical systems. Among these methods, are model development and validation processes such as parameter estimation, as well as Painleve and bifurcation analysis.     

Time delay in a basic model of the immune response

The effects of time delay on the two-dimensional system of Mayer et al., which represents the basic model of the immune response, are analysed (cf. Mayer H, Zaenker KS, an der Heiden U. A basic mathematical model of the immune response. Chaos, Solitons and Fractals 1995;5:155–61). We studied variations of the stability of the fixed points due to the time delay and the possibility for the occurrence of the chaotic solutions.     

Global dynamics of a spatial heterogeneous viral infection model with intracellular delay and nonlocal diffusion

In this paper, we propose a spatial heterogeneous viral infection model, where heterogeneous parameters, the intracellular delay and nonlocal diffusion of free virions are considered. The global well-posedness, compactness and asymptotic smoothness of the semiflow generated by the system are established. It is shown that the principal eigenvalue problem of a perturbation of the nonlocal diffusion operator has a principal eigenvalue associated with a positive eigenfunction. The principal eigenvalue plays the same role as the basic reproduction number being defined as the spectral radius of the next generation operator. The existence of the unique chronic-infection steady state is established by the super-sub solution method. Furthermore, the uniform persistence of the model is investigated by using the persistence theory of infinite dimensional dynamical systems. By setting the eigenfunction as the integral kernel of Lyapunov functionals, the global threshold dynamics of the system is established. More precisely, the infection-free steady state is globally asymptotically stable if the basic reproduction number is less than one; while the chronic-infection steady state is globally asymptotically stable if the basic reproduction number is larger than one. Numerical simulations are carried out to illustrate the effects of intracellular delay and diffusion rate on the final concentrations of infected cells and free virions, respectively.     

Global dynamics of a mathematical model for HTLV-I infection of CD4 T-cells

In this paper, a mathematical model for HILV-I infection of CD4⁺ T-cells is investigated. The force of infection is assumed be of a function in general form, and the resulting incidence term contains, as special cases, the bilinear and the saturation incidences. The model can be seen as an extension of the model [Wang et al. Mathematical analysis of the global dynamics of a model for HTLV-I infection and ATL progression, Math. Biosci. 179 (2002) 207-217; Song, Li, Global stability and periodic solution of a model for HTLV-I infection and ATL progression, Appl. Math. Comput. 180(1) (2006) 401-410]. Mathematical analysis establishes that the global dynamics of T-cells infection is completely determined by a basic reproduction number _R0${\mathfrak{R}}_0$. If _R0?1${\mathfrak{R}}_0?1$, the infection-free equilibrium is globally stable; if _R0>1${\mathfrak{R}}_0>1$, the unique infected equilibrium is globally stable in the interior of the feasible region.     

A fractional-order model of HIV infection with drug therapy effect

In this paper, the fractional-order model that describes HIV infection of CD4⁺ T cells with therapy effect is given. Generalized Euler Method (GEM) is employed to get numerical solution of such problem. The fractional derivatives are described in the Caputo sense.     

Global dynamics of a general brucellosis model with discrete delay

For the prevention and control of brucellosis, it is important to investigate the mechanism of brucellosis transmission. Based on the characteristics of the spread of brucellosis, a susceptible-exposed-infectious-brucella (SEIB) delay dynamic model is proposed with the general incidence, elimination rate and shedding rate of pathogen. Under biologically motivated assumptions, it shows the uniqueness of the endemic equilibrium, and investigates the global asymptotically stability of the disease-free equilibrium and the endemic equilibrium. The results suggest that the global stability of equilibria depends entirely on the basic reproduction number $R_0$ and time delay is harmless for the stability of equilibria. Finally, some specific examples and numerical simulations are used to illustrate the utilization of research results and reveal the biological significance of hypothesis $(H_7)$, which implies that the dynamics of brucellosis transmission depend largely on the development of the prevention and control strategies.     

The threshold for a stochastic HIV-1 infection model with Beddington-DeAngelis incidence rate

In this paper, we consider a stochastic HIV-1 infection model with Beddington-DeAngelis incidence rate. Before exploring its long-time behavior we show that there is a global positive solution of this model. Then sufficient conditions for extinction of the disease are established. Moreover, we give sufficient conditions for the existence of a stationary distribution of the model through constructing a suitable stochastic Lyapunov function. The stationary distribution implies that the disease is persistent in the mean. Therefore, a threshold value for the disease to disappear or prevail is obtained. Finally, some numerical examples are illustrated to support our theoretical results.     

Dynamics of an HIV-1 infection model with cell mediated immunity

In this paper, we study the dynamics of an improved mathematical model on HIV-1 virus with cell mediated immunity. This new 5-dimensional model is based on the combination of a basic 3-dimensional HIV-1 model and a 4-dimensional immunity response model, which more realistically describes dynamics between the uninfected cells, infected cells, virus, the CTL response cells and CTL effector cells. Our 5-dimensional model may be reduced to the 4-dimensional model by applying a quasi-steady state assumption on the variable of virus. However, it is shown in this paper that virus is necessary to be involved in the modeling, and that a quasi-steady state assumption should be applied carefully, which may miss some important dynamical behavior of the system. Detailed bifurcation analysis is given to show that the system has three equilibrium solutions, namely the infection-free equilibrium, the infectious equilibrium without CTL, and the infectious equilibrium with CTL, and a series of bifurcations including two transcritical bifurcations and one or two possible Hopf bifurcations occur from these three equilibria as the basic reproduction number is varied. The mathematical methods applied in this paper include characteristic equations, Routh–Hurwitz condition, fluctuation lemma, Lyapunov function and computation of normal forms. Numerical simulation is also presented to demonstrate the applicability of the theoretical predictions.     

Numerical resolution of an exact heat conduction model with a delay term

In this paper we analyze, from the numerical point of view, a dynamic thermoelastic problem. Here, the so-called exact heat conduction model with a delay term is used to obtain the heat evolution. Thus, the thermomechanical problem is written as a coupled system of partial differential equations, and its variational formulation leads to a system written in terms of the velocity and the temperature fields. An existence and uniqueness result is recalled. Then, fully discrete approximations are introduced by using the classical finite element method to approximate the spatial variable and the implicit Euler scheme to discretize the time derivatives. A priori error estimates are proved, from which the linear convergence of the algorithm could be derived under suitable additional regularity conditions. Finally, a two-dimensional numerical example is solved to show the accuracy of the approximation and the decay of the discrete energy.     

Global dynamics of a mathematical model for HTLV-I infection of CD4 T cells with delayed CTL response

Human T-cell leukaemia virus type I (HTLV-I) preferentially infects the CD4⁺ T cells. The HTLV-I infection causes a strong HTLV-I specific immune response from CD8⁺ cytotoxic T cells (CTLs). The persistent cytotoxicity of the CTL is believed to contribute to the development of a progressive neurologic disease, HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP). We investigate the global dynamics of a mathematical model for the CTL response to HTLV-I infection in vivo. To account for a series of immunological events leading to the CTL response, we incorporate a time delay in the response term. Our mathematical analysis establishes that the global dynamics are determined by two threshold parameters R₀ and R₁, basic reproduction numbers for viral infection and for CTL response, respectively. If R₀≤1, the infection-free equilibrium P₀ is globally asymptotically stable, and the HTLV-I viruses are cleared. If R₁≤1<R₀, the asymptomatic-carrier equilibrium P₁ is globally asymptotically stable, and the HTLV-I infection becomes chronic but with no persistent CTL response. If R₁>1, a unique HAM/TSP equilibrium P₂ exists, at which the HTLV-I infection is chronic with a persistent CTL response. We show that the time delay can destabilize the HAM/TSP equilibrium, leading to Hopf bifurcations and stable periodic oscillations. Implications of our results to the pathogenesis of HTLV-I infection and HAM/TSP development are discussed.     

Global dynamics of a discretized SIRS epidemic model with time delay

We derive a discretized SIRS epidemic model with time delay by applying a nonstandard finite difference scheme. Sufficient conditions for the global dynamics of the solution are obtained by improvements in discretization and applying proofs for continuous epidemic models. These conditions for our discretized model are the same as for the original continuous model.