Stability and Hopf bifurcation for a virus infection model with delayed humoral immunity response

In this paper, we investigate the dynamical behavior of a virus infection model with delayed humoral immunity. By using suitable Lyapunov functional and the LaSalle?s invariance principle, we establish the global stabilities of the two boundary equilibria. If _R0<1$R_0<1$, the uninfected equilibrium _E0$E_0$ is globally asymptotically stable; if _R1<1<_R0$R_1<1<R_0$, the infected equilibrium without immunity _E1$E_1$ is globally asymptotically stable. When _R1>1$R_1>1$, we obtain the sufficient conditions to the local stability of the infected equilibrium with immunity _E2$E_2$. The time delay can change the stability of _E2$E_2$ and lead to the existence of Hopf bifurcations. The stabilities of bifurcating periodic solutions is also studied. We check our theorems with numerical simulations in the end.     

Global stability of humoral immunity virus dynamics models with nonlinear infection rate and removal

In this paper, we investigate the dynamical behavior of two nonlinear models for viral infection with humoral immune response. The first model contains four compartments; uninfected target cells, actively infected cells, free virus particles and B cells. The intrinsic growth rate of uninfected cells, incidence rate of infection, removal rate of infected cells, production rate of viruses, neutralization rate of viruses, activation rate of B cells and removal rate of B cells are given by more general nonlinear functions. The second model is a modification of the first one by including an eclipse stage of infected cells. We assume that the latent-to-active conversion rate is also given by a more general nonlinear function. For each model we derive two threshold parameters and establish a set of conditions on the general functions which are sufficient to determine the global dynamics of the models. By using suitable Lyapunov functions and LaSalle’s invariance principle, we prove the global asymptotic stability of the all equilibria of the models. We perform some numerical simulations for the models with specific forms of the general functions and show that the numerical results are consistent with the theoretical results.     

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 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.     

Asymptotic behavior of a stochastic virus dynamics model with intracellular delay and humoral immunity

In this paper, we formulate a stochastic virus dynamics model with intracellular delay and humoral immunity. By constructing some suitable Lyapunov functions, we show that the solution of stochastic model is going around each of the steady states of the corresponding deterministic model under some conditions. Then, numerical simulations are given to support the theoretical results. Finally, we propose several more effective way to control the spread of the virus by analyzing the sensitivity of the threshold of spread.     

Global analysis of a multi-group animal epidemic model with indirect infection and time delay

The transmission mechanism of some animal diseases is complex because of the multiple transmission pathways and multiple-group interactions, which lead to the limited understanding of the dynamics of these diseases transmission. In this paper, a delay multi-group dynamic model is proposed in which time delay is caused by the latency of infection. Under the biologically motivated assumptions, the basic reproduction number $R_0$ is derived and then the global stability of the disease-free equilibrium and the endemic equilibrium is analyzed by Lyapunov functionals and a graph-theoretic approach as for time delay. The results show the global properties of equilibria only depend on the basic reproductive number $R_0$: the disease-free equilibrium is globally asymptotically stable if $R_0\leq 1$; if $R_0>1$, the endemic equilibrium exists and is globally asymptotically stable, which implies time delay span has no effect on the stability of equilibria. Finally, some specific examples are taken to illustrate the utilization of the results and then numerical simulations are used for further discussion. The numerical results show time delay model may experience periodic oscillation behaviors, implying that the spread of animal diseases depends largely on the prevention and control strategies of all sub-populations.     

Stability and Hopf bifurcation of a delayed virus infection model with Beddington–DeAngelis infection function and cytotoxic T‐lymphocyte immune response

In this paper, a class of virus infection model with Beddington–DeAngelis infection function and cytotoxic T‐lymphocyte immune response is investigated. Time delay in the immune response term is incorporated into the model. We show that the dynamics of the model are determined by the basic reproduction number and the immune response reproduction number . If , then the infection‐free equilibrium is globally asymptotically stable. If , then the immune‐free equilibrium is globally asymptotically stable. If , then the stability of the interior equilibrium is investigated. We conclude that Hopf bifurcation occurs as the time delay passes through a critical value. Numerical simulations are carried out to support our theoretical conclusion well. Copyright © 2015 John Wiley & Sons, Ltd.     

Stability of a general adaptive immunity virus dynamics model with multistages of infected cells and two routes of infection

This paper studies an (n+4)-dimensional nonlinear virus dynamics model that characterizes the interactions of the viruses, susceptible host cells, n-stages of infected cells, B cells and cytotoxic T lymphocyte (CTL) cells. Both viral and cellular infections have been incorporated into the model. The infected-susceptible and virus-susceptible infection rates as well as the generation and removal rates of all compartments are described by general nonlinear functions. Five threshold parameters are computed, which insure the existence of the equilibria of the model under consideration. A set of conditions on the general functions has been established, which is sufficient to investigate the global dynamics of the model. The global asymptotic stability of all equilibria is proven by utilizing Lyapunov function and LaSalle's invariance principle. The theoretical results are illustrated by numerical simulations of the model with specific forms of the general functions.     

具有Beddington-DeAngelis发生率和两个时滞的HIV感染模型的全局稳定性分析

研究了具有Beddington-DeAngelis发生率和细胞免疫反应的HIV模型的全局性.得到模型的基本再生数R_0和免疫基本再生数R_1.通过建立适当的Lyapunov函数,得出无病平衡点E_0,无免疫平衡点E_1和免疫平衡点E_2是全局渐近稳定的.     

Global stability and periodic oscillations for an SIV infection model with immune response and intracellular delays

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.     

Qualitative and bifurcation analysis using a computer virus model with a saturated recovery function

In this paper, we introduce a saturated treatment function into the computer virus propagation model, where the treatment function is limited for increasing number of infected computers. By carrying out global qualitative and bifurcation analysis, it is shown that the system exhibits some new and complicated behaviors: if the basic reproduction number is larger than unity, the number of infected computers will show persistent behavior, either converging to some positive constant or oscillating; and if the basic reproduction number is below unity, the model may exhibit complicated behaviors including: (i) backward bifurcation; (ii) almost sure virus eradication where the number of infective computers tends to zero for all initial positions except the interior equilibria; (iii) ‘‘oscillating’’ backward bifurcation where either the number of infective computers oscillates persistently, if the initial position lies in a region covering the stable virus equilibrium, or virus eradication, if the initial position lies outside this region; (iv) virus eradication for all initial positions if the basic reproduction number is less than a turning point value.     

Global properties for virus dynamics model with mitotic transmission and intracellular delay

In this paper we study the basic model of viral infections with mitotic transmission and intracellular delay discrete. The delay corresponds to the time between infection of uninfected cells and the emission of virus on a cellular level. By means of Volterra-type Lyapunov functionals, we provide the global stability for this model. Let η be the number of virus produced per infected cell. If ηcrit, the critical number, satisfies η?ηcrit, then the virus-free steady state is globally asymptotically stable. On the contrary if η>ηcrit, then the infected steady state is globally asymptotically stable if a sufficient condition is satisfied.     

Local and global stability analysis of a two prey one predator model with help

In this paper we propose and study a three dimensional continuous time dynamical system modelling a three team consists of two preys and one predator with the assumption that during predation the members of both teams of preys help each other and the rate of predation of both teams are different. In this work we establish the local asymptotic stability of various equilibrium points to understand the dynamics of the model system. Different conditions for the coexistence of equilibrium solutions are discussed. Persistence, permanence of the system and global stability of the positive interior equilibrium solution are discussed by constructing suitable Lyapunov functional. At the end, numerical simulations are performed to substantiate our analytical findings.     

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.     

Qualitative analysis of hepatitis B virus infection model with impulsive vaccination and time delay

According to the epidemic state, propagation mode and transformation between HBV infection states,the Hepatitis B Virus (HBV) infection with impulsive vaccination and time delay are modelled and analyzed. The control methods of impulsive vaccination and active therapy are adopted. By using comparative theorem of impulsive differential equation, the sufficient conditions that Hepatitis B Virus will be eliminated eventually or be persistent are derived.     

Analysis of a nonautonomous dynamical model of diseases through droplet infection and direct contact

In this paper, we have considered a nonautonomous dynamical model of diseases that spread by droplet infection and also through direct contact (with a lower risk) with varying total population size and distributed time delay to become infectious. It is assumed that there is a time lag due to incubation period of pathogens, i.e. the development of an infection from the time the pathogen enters the body until signs or symptoms first appear. Here, we have established some sufficient conditions on the permanence and extinction of the disease by using inequality analytical technique. We have obtained the explicit formula of the eventual lower bounds of infected persons. We have introduced some new threshold values. By Lyapunov functional method, we have also obtained some sufficient conditions for global asymptotic stability of this model. Computer simulations are carried out to explain the analytical findings. The aim of the analysis of this model is to trace the parameters of interest for further study, with a view to informing and assisting policy-maker in targeting prevention and treatment resources for maximum effectiveness.     

Stability of a general delay‐distributed virus dynamics model with multi‐staged infected progression and immune response

In this paper, we formulate a (n + 3)‐dimensional nonlinear virus dynamics model that considers n‐stages of the infected cells and n + 1 distributed time delays. The model incorporates humoral immune response and general nonlinear forms for the incidence rate of infection, the generation and removal rates of the cells and viruses. Under a set of conditions on the general functions, the basic infection reproduction number and the humoral immune response activation number are derived. Utilizing Lyapunov functionals and LaSalle's invariance principle, the global asymptotic stability of all steady states of the model are proven. Numerical simulations are carried out to confirm the theoretical results. Copyright © 2016 John Wiley & Sons, Ltd.