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.     

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.     

Global dynamics of an age‐structured virus model with saturation effects

An infection‐age virus dynamics model for human immunodeficiency virus (or hepatitis B virus) infections with saturation effects of infection rate and immune response is investigated in this paper. It is shown that the global dynamics of the model is completely determined by two critical values R ₀, the basic reproductive number for viral infection, and R ₁, the viral reproductive number at the immune‐free infection steady state (R ₁<R ₀). If R ₀<1, the uninfected steady state E ⁰ is globally asymptotically stable; if R ₀>1 > R ₁, the immune‐free infected steady state E ^? is globally asymptotically stable; while if R ₁>1, the antibody immune infected steady state is globally asymptotically stable. Moreover, our results show that ignoring the saturation effects of antibody immune response or infection rate will result in an overestimate of the antibody immune reproductive number. Copyright © 2016 John Wiley & Sons, Ltd.     

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.     

Mathematical model for the dynamics of visceral leishmaniasis–malaria co‐infection

A mathematical model to understand the dynamics of malaria–visceral leishmaniasis co‐infection is proposed and analyzed. Results show that both diseases can be eliminated if R₀, the basic reproduction number of the co‐infection, is less than unity, and the system undergoes a backward bifurcation where an endemic equilibrium co‐exists with the disease‐free equilibrium when one of R_m or R_l, the basic reproduction numbers of malaria‐only and visceral leishmaniasis‐only, is precisely less than unity. Results also show that in the case of maximum protection against visceral leishmaniasis (VL), the disease‐free equilibrium is globally asymptotically stable if malaria patients are protected from VL infection; similarly, in the case of maximum protection against malaria, the disease‐free equilibrium is globally asymptotically stable if VL and post‐kala‐azar dermal leishmaniasis patients and the recovered humans after VL are protected from malaria infection. Numerical results show that if R_m and R_l are greater than unity, then we have co‐existence of both disease at an endemic equilibrium, and malaria incidence is higher than visceral leishmaniasis incidence at steady state. Copyright © 2016 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 a stage-structured epidemic model with a nonlinear incidence

In this paper, a stage-structured epidemic model with a nonlinear incidence with a factor S^p is investigated. By using limit theory of differential equations and Theorem of Busenberg and van den Driessche, global dynamics of the model is rigorously established. We prove that if the basic reproduction number R₀ is less than one, the disease-free equilibrium is globally asymptotically stable and the disease dies out; if R₀ is greater than one, then the disease persists and the unique endemic equilibrium is globally asymptotically stable. Numerical simulations support our analytical results and illustrate the effect of p on the dynamic behavior of the model.     

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.     

Global stability of multi-group epidemic models with distributed delays

We investigate a class of multi-group epidemic models with distributed delays. We establish that the global dynamics are completely determined by the basic reproduction number R₀. More specifically, we prove that, if R₀?1, then the disease-free equilibrium is globally asymptotically stable; if R₀>1, then there exists a unique endemic equilibrium and it is globally asymptotically stable. Our proof of global stability of the endemic equilibrium utilizes a graph-theoretical approach to the method of Lyapunov functionals.     

Global stability of nonresident computer virus models

In this paper, applying Lyapunov functional techniques to nonresident computer virus models, we establish global dynamics of the model whose threshold parameter is the basic reproduction number R₀ such that the virus‐free equilibrium is globally asymptotically stable when R₀ ≤ 1, and the infected equilibrium is globally asymptotically stable when R₀ > 1 under the same restricted condition on a parameter, which appeared in the literature on delayed susceptible‐infected‐recovered‐susceptible (SIRS) epidemic models. We use new techniques on permanence and global stability of this model for R₀ > 1. Copyright © 2014 John Wiley & Sons, Ltd.     

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

In this paper, we introduce a basic reproduction number for a multigroup SEIR model with nonlinear incidence of infection and nonlinear removal functions between compartments. Then, we establish that global dynamics are completely determined by the basic reproduction number R₀. It shows that, the basic reproduction number R₀ is a global threshold parameter in the sense that if it is less than or equal to one, the disease free equilibrium is globally stable and the disease dies out; whereas if it is larger than one, there is a unique endemic equilibrium which is globally stable and thus the disease persists in the population. Finally, two numerical examples are also included to illustrate the effectiveness of the proposed result.     

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.     

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.     

Analysis of a viral infection model with immune impairment,intracellular delay and general non-linear incidence rate

In this article we study the dynamical behaviour of a intracellular delayed viral infection with immune impairment model and general non-linear incidence rate. Several techniques, including a non-linear stability analysis by means of the Lyapunov theory and sensitivity analysis, have been used to reveal features of the model dynamics. The classical threshold for the basic reproductive number is obtained: if the basic reproductive number of the virus is less than one, the infection-free equilibrium is globally asymptotically stable and the infected equilibrium is globally asymptotically stable if the basic reproductive number is higher than one.     

Global properties of a class of HIV infection models with Beddington–DeAngelis functional response

In this paper, the global properties of a class of human immunodeficiency virus (HIV) models with Beddington–DeAngelis functional response are investigated. Lyapunov functions are constructed to establish the global asymptotic stability of the uninfected and infected steady states of three HIV infection models. The first model considers the interaction process of the HIV and the CD4 ⁺ T cells and takes into account the latently and actively infected cells. The second model describes two co‐circulation populations of target cells, representing CD4 ⁺ T cells and macrophages. The third model is a two‐target‐cell model taking into account the latently and actively infected cells. We have proven that if the basic reproduction number R₀ is less than unity, then the uninfected steady state is globally asymptotically stable, and if R₀ > 1, then the infected steady state is globally asymptotically stable. Copyright © 2012 John Wiley & Sons, Ltd.     

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.     

一类具免疫应答和非线性感染函数的时滞HIV-1感染模型的全局稳定性

考虑到HIV-1感染过程中免疫反应和非线性感染函数,建立了一类具有三个分布时滞的HIV-1感染动力学模型.得到了关于病毒感染的基本再生数R0和CTLs免疫反应的基本再生数R1 ＜R0.通过构造Lyapunov泛函证明了系统具有阈值动力学性质,即当R0≤1时,系统存在全局渐近稳定的无感染平衡点;当R1≤1＜R0时,系统出...     

Stability of a delayed SIRS epidemic model with a nonlinear incidence rate

In this paper, an SIRS epidemic model with a nonlinear incidence rate and a time delay is investigated. By analyzing the corresponding characteristic equations, the local stability of an endemic equilibrium and a disease-free equilibrium is discussed. By comparison arguments, it is proved that if the basic reproductive number R₀<1, the disease-free equilibrium is globally asymptotically stable. If R₀>1, by means of an iteration technique, sufficient conditions are derived for the global asymptotic stability of the endemic equilibrium.     

Global analysis of a vector-host epidemic model with nonlinear incidences

In this paper, an epidemic model with nonlinear incidences is proposed to describe the dynamics of diseases spread by vectors (mosquitoes), such as malaria, yellow fever, dengue and so on. The constant human recruitment rate and exponential natural death, as well as vector population with asymptotically constant population, are incorporated into the model. The stability of the system is analyzed for the disease-free and endemic equilibria. The stability of the system can be controlled by the threshold number R₀. It is shown that if R₀ is less than one, the disease free equilibrium is globally asymptotically stable and in such a case the endemic equilibrium does not exist; if R₀ is greater than one, then the disease persists and the unique endemic equilibrium is globally asymptotically stable. Our results imply that the threshold condition of the system provides important guidelines for accessing control of the vector diseases, and the spread of vector epidemic in an efficient way can be prevented. The contribution of the nonlinear saturating incidence to the basic reproduction number and the level of the endemic equilibrium are also analyzed, respectively.