Global dynamics of a viral infection model with a latent period and Beddington-DeAngelis response

In this paper, we study the global dynamics of a viral infection model with a latent period. The model has a nonlinear function which denotes the incidence rate of the virus infection in vivo. The basic reproduction number of the virus is identified and it is shown that the uninfected equilibrium is globally asymptotically stable if the basic reproduction number is equal to or less than unity. Moreover, the virus and infected cells eventually persist and there exists a unique infected equilibrium which is globally asymptotically stable if the basic reproduction number is greater than unity. The basic reproduction number determines the equilibrium that is globally asymptotically stable, even if there is a time delay in the infection.     

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.     

Global stability analysis and permanence for an HIV-1 dynamics model with distributed delays

This paper mainly investigates the global asymptotic stabilities of two HIV dynamics models with two distributed intracellular delays incorporating Beddington-DeAngelis functional response infection rate. An eclipse stage of infected cells (i.e. latently infected cells), not yet producing virus, is included in our models. For the first model, it is proven that if the basic reproduction number $R_0$ is less than unity, then the infection-free equilibrium is globally asymptotically stable, and if $R_0 $ is greater than unity, then the infected equilibrium is globally asymptotically stable. We also obtain that the disease is always present when $R_0 $ is greater than unity by using a permanence theorem for infinite dimensional systems. What is more, a n-stage-structured HIV model with two distributed intracellular delays, which is the extensions to the first model, is developed and analyzed. We also prove the global asymptotical stabilities of two equilibria by constructing suitable Lyapunov functionals.     

Global properties of an improved hepatitis B virus model

Hepatitis B virus (HBV) infection is an important health problem worldwide. In this paper, we introduce an improved HBV model with standard incidence function and cytokine-mediated ‘cure’ based on empirical evidences. By carrying out a global analysis of the modified model and studying the stability of the equilibria, we show that infection-free equilibrium is globally asymptotically stable if the basic reproduction number of virus is less than one and, conversely, the infection equilibrium is globally asymptotically stable if the basic reproduction number of virus is greater than one. The study and information derived from this model and other related models may have an important impact on preventing mortality due to hepatitis B virus in the future.     

一类具有分布时滞和非线性发生率的媒介传染病模型的全局稳定性

建立了一类具有分布时滞和非线性发生率的SIR媒介传染病模型,分析得到了决定疾病是否一致持续存在的基本再生数．而且当基本再生数不大于1时,疾病最终灭绝;当基本再生数大于1时,模型存在惟一的地方病平衡点,并且疾病一致持续存在于种群之中．通过构造Lyapunov泛函,证明了在一定条件下地方病平衡点只要存在就全局稳定．同时指出了证明地方病平衡点全局稳定时可适用的Lyapunov泛函的不惟一性.     

A class of Lyapunov functions and the global stability of some epidemic models with nonlinear incidence

In this paper, by investigating an SIR epidemic model with nonlinear incidence, we present a new technique for proving the global stability of the endemic equilibrium, which consists of introducing a variable transformation and constructing a more general Lyapunov function. For the model we obtain the following results. The disease-free equilibrium is globally stable in the feasible region as the basic reproduction number is less than or equal to unity, and the endemic equilibrium is globally stable in the feasible region as the basic reproduction number is greater than unity.The generality of the technique is illustrated by considering certain nonlinear incidences and SIS and SIRS epidemic models.     

Stability and Hopf Bifurcation of a Virus Infection Model with a Delayed CTL Immune Response

In this paper, a virus infection model with standard incidence rate and delayed CTL immune response is investigated. By analyzing corresponding characteristic equations, the local stability of each of feasible equilibria and the existence of Hopf bifurcations at the CTL-activated infection equilibrium are established, respectively. By means of comparison arguments, it is verified that the infection-free equilibrium is globally asymptotically stable if the basic reproduction ratio is less than unity. By using suitable Lyapunov functional and LaSalle＇s invariance principle, it is shown that the CTL-inactivated infection equilibrium of the system is globally asymptotically stable if tile immune response reproduction ratio is less than unity and the basic reproduction ratio is greater than unity. Numerical simulations are carried out to illustrate the theoretical result.     

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...     

一类具有双线性传染率的HIV/AIDS病毒动力学改进模型

针对HIV/AIDS传播的具有常数移民和指数出生的SI型模型,为了更加符合实际意义,对具有双线性传染率的模型进行局部改进,并对改进后的动力学模型进行了简化.对于改进后的模型,证明了平衡点的存在与局部稳定性,并证明了传染病毒的灭绝与持续性,得到了传染病毒的基本再生数.结果表明:当单位时间内从外界迁入人口中染病者的比例系数c近似等于零时,基本再生数小于1时,传染病毒最终灭绝;当基本再生数大于1时,模型存在唯一的正平衡点,且是局部渐近稳定的,说明传染病毒一致持续存在.     

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.     

Lyapunov functions for a dengue disease transmission model

In this paper, we study a model for the dynamics of dengue fever when only one type of virus is present. For this model, Lyapunov functions are used to show that when the basic reproduction ratio is less than or equal to one, the disease-free equilibrium is globally asymptotically stable, and when it is greater than one there is an endemic equilibrium which is also globally asymptotically stable.     

Stability and bifurcation analysis of a viral infection model with delayed immune response

In this paper, we study a viral infection model with an immunity time delay accounting for the time between the immune system touching antigenic stimulation and generating CTLs. By calculation, we derive two thresholds to determine the global dynamics of the model, i.e., the reproduction number for viral infection $R_{0}$ and for CTL immune response $R_{1}$. By analyzing the characteristic equation, the local stability of each feasible equilibrium is discussed. Furthermore, the existence of Hopf bifurcation at the CTL-activated infection equilibrium is also studied. By constructing suitable Lyapunov functionals, we prove that when $R_{0}\leq1$, the infection-free equilibrium is globally asymptotically stable; when $R_{0}>1$ and $R_{1}\leq1$, the CTL-inactivated infection equilibrium is globally asymptotically stable; Numerical simulation is carried out to illustrate the main results in the end.     

Global stability of epidemiological models with group mixing and nonlinear incidence rates

For a multigroup SEIR epidemiological model with nonlinear incidence rates, the basic reproduction number is identified. It is shown that, under certain group mixing patterns and nonlinearity and/or nonsmoothness in the incidence of infection, the basic reproduction number is a global threshold parameter in the sense that the disease free equilibrium is globally stable if the basic reproduction number is less than one and the endemic equilibrium is globally stable if the basic reproduction number is greater than one.     

Global dynamics of delay‐distributed HIV infection models with differential drug efficacy in cocirculating target cells

In this paper, we investigate the dynamical behaviors of three human immunodeficiency virus infection models with two types of cocirculating target cells and distributed intracellular delay. The models take into account both short‐lived infected cells and long‐lived chronically infected cells. In the two types of target cells, the drug efficacy is assumed to be different. The incidence rate of infection is given by bilinear and saturation functional responses in the first and second models, respectively, while it is given by a general function in the third model. Lyapunov functionals are constructed and LaSalle invariance principle is applied to prove the global asymptotic stability of all equilibria of the models. We have derived the basic reproduction number R₀ for the three models. For the first two models, we have proven that the disease‐free equilibrium is globally asymptotically stable (GAS) when R₀≤1, and the endemic equilibrium is GAS when R₀>1. For the third model, we have established a set of sufficient conditions for global stability of both equilibria of the model. We have checked our theoretical results with numerical simulations. Copyright © 2015 John Wiley & Sons, Ltd.     

Long term dynamics in a mathematical model of HIV-1 infection with delay in different variants of the basic drug therapy model

Infection with HIV-1, degrading the human immune system and recent advances of drug therapy to arrest HIV-1 infection, has generated considerable research interest in the area. Bonhoeffer et al. (1997) [1], introduced a population model representing long term dynamics of HIV infection in response to available drug therapies. We consider a similar type of approximate model incorporating time delay in the process of infection on the healthy T cells which, in turn, implies inclusion of a similar delay in the process of viral replication. The model is studied both analytically and numerically. We also include a similar delay in the killing rate of infected CD4⁺ T cells by Cytotoxic T-Lymphocyte (CTL) and in the stimulation of CTL and analyse two resulting models numerically.The models with no time delay present have two equilibria: one where there is no infection and a non-trivial equilibrium where the infection can persist. If there is no time delay then the non-trivial equilibrium is locally asymptotically stable. Both our analytical results (for the first model) and our numerical results (for all three models) indicate that introduction of a time delay can destabilize the non-trivial equilibrium. The numerical results indicate that such destabilization occurs at realistic time delays and that there is a threshold time delay beneath which the equilibrium with infection present is locally asymptotically stable and above which this equilibrium is unstable and exhibits oscillatory solutions of increasing amplitude.     

Lytic cycle: A defining process in oncolytic virotherapy

The viral lytic cycle is an important process in oncolytic virotherapy. Most mathematical models for oncolytic virotherapy do not incorporate this process. In this article, we propose a mathematical model with the viral lytic cycle based on the basic mathematical model for oncolytic virotherapy. The viral lytic cycle is characterized by two parameters, the time period of the viral lytic cycle and the viral burst size. The time period of the viral lytic cycle is modeled as a delay parameter. The model is a nonlinear system of delay differential equations. The model reveals a striking feature that the critical value of the period of the viral lytic cycle is determined by the viral burst size. There are two threshold values for the burst size. Below the first threshold, the system has an unstable trivial equilibrium and a globally stable virus free equilibrium for any nonnegative delay, while the system has a third positive equilibrium when the burst size is greater than the first threshold. When the burst size is above the second threshold, there is a functional relation between the bifurcation value of the delay parameter for the period of the viral lytic cycle and the burst size. If the burst size is greater than the second threshold, the positive equilibrium is stable when the period of the viral lytic cycle is smaller than the bifurcation value, while the system has orbitally stable periodic solutions when the period of the lytic cycle is longer than the bifurcation value. However, this bifurcation value becomes smaller when the burst size becomes bigger. The viral lytic cycle may explain the oscillation phenomena observed in many studies. An important clinic implication is that the burst size should be carefully modified according to its effect on the lytic cycle when a type of a virus is modified for virotherapy, so that the period of the viral lytic cycle is in a suitable range which can break away the stability of the positive equilibria or periodic solutions.     

Stability Analysis of an SEIS Epidemic Model with Nonlinear Incidence and Time Delay

In this paper, an SEIS epidemic model with nonlinear incidence and time delay is investigated. By analyzing the corresponding characteristic equations, the local stability of each of feasible equilibria of the model is established. By using suitable Lyapunov functional and LaSalle's invariance principle, it is shown that the disease-free equilibrium is globally asymptotically stable if the basic reproduction number is less than unity. If the basic reproduction number is greater than unity, by means of an iteration technique, sufficient conditions are derived for the global stability of the endemic equilibrium. Numerical simulations are carried out to illustrate the theoretical results.