Global analysis of virus dynamics model with logistic mitosis,cure rate and delay in virus production

In this paper, we study a virus dynamics model with logistic mitosis, cure rate, and intracellular delay. By means of construction of a suitable Lyapunov functionals, obtained by linear combinations of Volterra—type functions, composite quadratic functions and Volterra—type functionals, we provide the global stability for this model. If R₀, the basic reproductive number, satisfies R₀ ≤ 1, then the infection‐free equilibrium state is globally asymptotically stable. Our system is persistent if R₀ > 1. On the other hand, if R₀ > 1, then infection‐free equilibrium becomes unstable and a unique infected equilibrium exists. The local stability analysis is carried out for the infected equilibrium, and it is shown that, if the parameters satisfy a condition, the infected equilibrium can be unstable and a Hopf bifurcation can occur. We also have that if R₀ > 1, then the infected equilibrium state is globally asymptotically stable if a sufficient condition is satisfied. We illustrate our findings with some numerical simulations. Copyright © 2014 John Wiley & Sons, Ltd.     

Global dynamics of a cell mediated immunity in viral infection models with distributed delays

In this paper, we investigate global dynamics for a system of delay differential equations which describes a virus-immune interaction in vivo. The model has two distributed time delays describing time needed for infection of cell and virus replication. Our model admits three possible equilibria, an uninfected equilibrium and infected equilibrium with or without immune response depending on the basic reproduction number for viral infection R₀ and for CTL response R₁ such that R₁<R₀. It is shown that there always exists one equilibrium which is globally asymptotically stable by employing the method of Lyapunov functional. More specifically, the uninfected equilibrium is globally asymptotically stable if R₀?1, an infected equilibrium without immune response is globally asymptotically stable if R₁?1<R₀ and an infected equilibrium with immune response is globally asymptotically stable if R₁>1. The immune activation has a positive role in the reduction of the infection cells and the increasing of the uninfected cells if R₁>1.     

A differential equation model of HIV infection of CD4T-cells with cure rate

A differential equation model of HIV infection of CD4⁺T-cells with cure rate is studied. We prove that if the basic reproduction number R₀<1, the HIV infection is cleared from the T-cell population and the disease dies out; if R₀>1, the HIV infection persists in the host. We find that the chronic disease steady state is globally asymptotically stable if R₀>1. Furthermore, we also obtain the conditions for which the system exists an orbitally asymptotically stable periodic solution. Numerical simulations are presented to illustrate the results.     

Global stability of a virus dynamics model with intracellular delay and CTL immune response

In this paper, the global stability of a virus dynamics model with intracellular delay, Crowley–Martin functional response of the infection rate, and CTL immune response is studied. By constructing suitable Lyapunov functions and using LaSalles invariance principle, the global dynamics is established; it is proved that if the basic reproductive number, R₀, is less than or equal to one, the infection‐free equilibrium is globally asymptotically stable; if R₀ is more than one, and if immune response reproductive number, R⁰, is less than one, the immune‐free equilibrium is globally asymptotically stable, and if R⁰ is more than one, the endemic equilibrium is globally asymptotically stable. Copyright © 2014 John Wiley & Sons, Ltd.     

Global dynamics of a Vector‐Borne disease model with two delays and nonlinear transmission rate

In this paper, we investigate a Vector‐Borne disease model with nonlinear incidence rate and 2 delays: One is the incubation period in the vectors and the other is the incubation period in the host. Under the biologically motivated assumptions, we show that the global dynamics are completely determined by the basic reproduction number R₀. The disease‐free equilibrium is globally asymptotically stable if R₀≤1; when R₀>1, the system is uniformly persistent, and there exists a unique endemic equilibrium that is globally asymptotically. Numerical simulations are conducted to illustrate the theoretical results.     

Global stability of delay multigroup epidemic models with group mixing and nonlinear incidence rates

In this paper, we present a new delay multigroup SEIR model with group mixing and nonlinear incidence rates and investigate its global stability. We establish that the global dynamics of the models are completely determined by the basic reproduction number R₀. It is shown that, if R₀?1, then the disease free equilibrium is globally asymptotically stable and the disease dies out; if R₀>1, there exists a unique endemic equilibrium that is globally asymptotically stable and thus the disease persists in the population. Finally, a numerical example is also discussed to illustrate the effectiveness of the results.     

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.     

Analysis of an SVEIS epidemic model with partial temporary immunity and saturation incidence rate

In this paper, an SVEIS epidemic model for an infectious disease that spreads in the host population through horizontal transmission is investigated. The role that temporary immunity (natural, disease induced, vaccination induced) plays in the spread of disease, is incorporated in the model. The total host population is bounded and the incidence term is of the Holling-type II form. It is shown that the model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. The global dynamics are completely determined by the basic reproduction number R₀. If R₀<1, the disease-free equilibrium is globally stable which leads to the eradication of disease from population. If R₀>1, a unique endemic equilibrium exists and is globally stable in the feasible region under certain conditions. Further, the transcritical bifurcation at R₀=1 is explored by projecting the flow onto the extended center manifold. We use the geometric approach for ordinary differential equations which is based on the use of higher-order generalization of Bendixson’s criterion. Further, we obtain the threshold vaccination coverage required to eradicate the disease. Finally, taking biologically relevant parametric values, numerical simulations are performed to illustrate and verify the analytical results.     

A delayed computer virus propagation model and its dynamics

In this paper, we propose a delayed computer virus propagation model and study its dynamic behaviors. First, we give the threshold value R₀ determining whether the virus dies out completely. Second, we study the local asymptotic stability of the equilibria of this model and it is found that, depending on the time delays, a Hopf bifurcation may occur in the model. Next, we prove that, if R₀ = 1, the virus-free equilibrium is globally attractive; and when R₀ < 1, it is globally asymptotically stable. Finally, a sufficient criterion for the global stability of the virus equilibrium is obtained.     

Dynamics of SIS model with saturation incidence,infection age and impulsive birth

In this paper, an impulsive birth and infection age SIS epidemic model is studied. Since infection age is an important factor of epidemic progression, we incorporate the infection age into the model. In this model, we analyze the dynamical behaviors of this model and point out that there exists an infection‐free periodic solution that is globally asymptotically stable if R₀<1. When R₁>1, R₂<1, then the disease is permanent. Our results indicate that a large period T of pulse, or a small pulse birth rate p is the sufficient condition for the eradication of the disease. Copyright © 2009 John Wiley & Sons, Ltd.     

Stability analysis of predator–prey system with migrating prey and disease infection in both species

We formulated and studied a predator–prey system with migrating prey and disease infection in both species. We used Lotka–Volterra type functional response. Mathematically, we analyzed the dynamics of the system such as existence of non negative equilibria, their stability. The basic reproduction number R₀ for the proposed mathematical model is calculated. Disease is endemic if R₀ > 1. Model is simulated by assuming hypothetical initial values and parameters.     

Global dynamics of a intracellular infection model with delays and humoral immunity

A virus infection model with time delays and humoral immunity has been investigated. Mathematical analysis shows that the global dynamics of the model is fully determined by the basic reproduction numbers of the virus and the immune response, R₀ and R₁. The infection‐free equilibrium P₀ is globally asymptotically stable when R₀≤1. The infection equilibrium without immunity P₁ is globally asymptotically stable when R₁≤1 < R₀. The infection equilibrium with immunity P₂ is globally asymptotically stable when R₁>1. The expression of the basic reproduction number of the immune response R₁ implies that the immune response reduces the concentration of free virus as R₁>1. Copyright © 2016 John Wiley & Sons, Ltd.     

Analysis of a SEIV epidemic model with a nonlinear incidence rate

In this paper, a SEIV epidemic model with a nonlinear incidence rate is investigated. The model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. It is shown that if the basic reproduction number _R0<1${\mathfrak{R}}_0<1$, the disease-free equilibrium is globally asymptotically stable and in such a case the endemic equilibrium does not exist. Moreover, we show that if the basic reproduction number _R0>1${\mathfrak{R}}_0>1$, the disease is uniformly persistent and the unique endemic equilibrium of the system with saturation incidence is globally asymptotically stable under certain conditions.     

Global dynamics of a multistage SIR model with distributed delays and nonlinear incidence rate

In this paper, a multistage susceptible‐infectious‐recovered model with distributed delays and nonlinear incidence rate is investigated, which extends the model considered by Guo et al. [H. Guo, M. Y. Li and Z. Shuai, Global dynamics of a general class of multistage models for infectious diseases, SIAM J. Appl. Math., 72 (2012), 261–279]. Under some appropriate and realistic conditions, the global dynamics is completely determined by the basic reproduction number R₀. If R₀≤1, then the infection‐free equilibrium is globally asymptotically stable and the disease dies out in all stages. If R₀>1, then a unique endemic equilibrium exists, and it is globally asymptotically stable, and hence the disease persists in all stages. The results are proved by utilizing the theory of non‐negative matrices, Lyapunov functionals, and the graph‐theoretical approach. Copyright © 2016 John Wiley & Sons, Ltd.     

A class of delayed viral models with saturation infection rate and immune response

In this paper, a class of three delayed viral dynamics models with immune response and saturation infection rate are proposed and studied. By constructing suitable Lyapunov functionals, we derive the basic reproduction number R₀ and the corresponding immune response reproduction numbers for the viral infection models, and establish that the global dynamics are completely determined by the values of the related basic reproduction number and immune response reproduction numbers. Copyright © 2012 John Wiley & Sons, Ltd.     

Global stability for an HIV/AIDS epidemic model with different latent stages and treatment

An HIV/AIDS epidemic model with different latent stages and treatment is constructed. The model allows for the latent individuals to have the slow and fast latent compartments. Mathematical analyses establish that the global dynamics of the spread of the HIV infectious disease are determined by the basic reproduction number under some conditions. If R₀ < 1, the disease free equilibrium is globally asymptotically stable, and if R₀ > 1, the endemic equilibrium is globally asymptotically stable for a special case. Some numerical simulations are also carried out to confirm the analytical results.     

Global stability of multi-group SEIR epidemic models with distributed delays and nonlinear transmission

The dynamics of multi-group SEIR epidemic models with distributed and infinite delay and nonlinear transmission are investigated. We derive the basic reproduction number R₀ and establish that the global dynamics are completely determined by the values of R₀: if R₀≤1, then the disease-free equilibrium is globally asymptotically stable; if R₀>1, then there exists a unique endemic equilibrium which is globally asymptotically stable. Our results contain those for single-group SEIR models with distributed and infinite delays. In the proof of global stability of the endemic equilibrium, we exploit a graph-theoretical approach to the method of Lyapunov functionals. The biological significance of the results is also discussed.     

On global stability of the intra-host dynamics of malaria and the immune system

In this paper we consider an intra-host model for the dynamics of malaria. The model describes the dynamics of the blood stage malaria parasites and their interaction with host cells, in particular red blood cells (RBC) and immune effectors. We establish the equilibrium points of the system and analyze their stability using the theory of competitive systems, compound matrices and stability of periodic orbits. We established that the disease-free equilibrium is globally stable if and only if the basic reproduction number satisfies R₀?1 and the parasite will be cleared out of the host. If R₀>1, a unique endemic equilibrium is globally stable and the parasites persist at the endemic steady state. In the presence of the immune response, the numerical analysis of the model shows that the endemic equilibrium is unstable.