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 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 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 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 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.     

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 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.     

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 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 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.     

Stability analysis of a virus infection model with humoral immunity response and two time delays

In this paper, we investigate the dynamical properties for a model of delay differential equations, which describes a virus‐immune interaction in vivo. By analyzing corresponding characteristic equations, the local stability of the equilibria for infection‐free, antibody‐free, and antibody response and the existence of Hopf bifurcation with antibody response delay as a bifurcation parameter at the antibody‐activated infection equilibrium are established, respectively. Global stability of the equilibria for infection‐free, antibody‐free, and antibody response, respectively, also are established by applying the Lyapunov functionals method. The numerical simulations are performed in order to illustrate the dynamical behavior of the model. 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.     

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.     

An epidemic model of a vector-borne disease with direct transmission and time delay

This paper considers an epidemic model of a vector-borne disease which has direct mode of transmission in addition to the vector-mediated transmission. The incidence term is assumed to be of the bilinear mass-action form. We include both a baseline ODE version of the model, and, a differential-delay model with a discrete time delay. The ODE model shows that the dynamics is completely determined by the basic reproduction number R₀. If R₀?1, the disease-free equilibrium is globally stable and the disease dies out. If R₀>1, a unique endemic equilibrium exists and is locally asymptotically stable in the interior of the feasible region. The delay in the differential-delay model accounts for the incubation time the vectors need to become infectious. We study the effect of that delay on the stability of the equilibria. We show that the introduction of a time delay in the host-to-vector transmission term can destabilize the system and periodic solutions can arise through Hopf bifurcation.     

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.     

Qualitative analysis of the SICR epidemic model with impulsive vaccinations

Control of epidemic infections is a very urgent issue today. To develop an appropriate strategy for vaccinations and effectively prevent the disease from arising and spreading, we proposed a modified Susceptible‐Infected‐Removed model with impulsive vaccinations. For the model without vaccinations, we proved global stability of one of the steady states depending on the basic reproduction number R₀. As typically in the epidemic models, the threshold value of R₀ is 1. If R₀ is greater than 1, then the positive steady state called endemic equilibrium exists and is globally stable, whereas for smaller values of R₀, it does not exist, and the semi‐trivial steady state called disease‐free equilibrium is globally stable. Using impulsive differential equation comparison theorem, we derived sufficient conditions under which the infectious disease described by the considered model disappears ultimately. The analytical results are illustrated by numerical simulations for Hepatitis B virus infection that confirm the theoretical possibility of the infection elimination because of the proper vaccinations policy. Copyright © 2012 John Wiley & Sons, Ltd.     

Stability analysis in a diffusional immunosuppressive infection model with delayed antiviral immune response

In this paper, the diffusion is introduced to an immunosuppressive infection model with delayed antiviral immune response. The direction and stability of Hopf bifurcation are effected by time delay, in the absence of which the positive equilibrium is locally asymptotically stable by means of analyzing eigenvalue spectrum; however, when the time delay increases beyond a threshold, the positive equilibrium loses its stability via the Hopf bifurcation. The stability and direction of the Hopf bifurcation is investigated with the norm form and the center manifold theory. The stability of the Hopf bifurcation leads to the emergence of spatial spiral patterns. Numerical calculations are performed to illustrate our theoretical results. Copyright © 2017 John Wiley & Sons, Ltd.     

Modelling the effect of tuberculosis on the spread of HIV infection in a population with density-dependent birth and death rate

A nonlinear mathematical model is proposed to study the effect of tuberculosis on the spread of HIV infection in a logistically growing human population. The host population is divided into four sub classes of susceptibles, TB infectives, HIV infectives (with or without TB) and that of AIDS patients. The model exhibits four equilibria namely, a disease free, HIV free, TB free and an endemic equilibrium. The model has been studied qualitatively using stability theory of nonlinear differential equations and computer simulation. We have found a threshold parameter R₀ which is if less than one, the disease free equilibrium is locally asymptotically stable otherwise for R₀>1, at least one of the infections will be present in the population. It is shown that the positive endemic equilibrium is always locally stable but it may become globally stable under certain conditions showing that the disease becomes endemic. It is found that as the number of TB infectives decreases due to recovery, the number of HIV infectives also decreases and endemic equilibrium tends to TB free equilibrium. It is also observed that number of AIDS individuals decreases if TB is not associated with HIV infection. A numerical study of the model is also performed to investigate the influence of certain key parameters on the spread of the disease.     

Dynamical behavior of computer virus on Internet

In this paper, we presented a computer virus model using an SIRS model and the threshold value R₀ determining whether the disease dies out is obtained. If R₀ is less than one, the disease-free equilibrium is globally asymptotically stable. By using the time delay as a bifurcation parameter, the local stability and Hopf bifurcation for the endemic state is investigated. Numerical results demonstrate that the system has periodic solution when time delay is larger than a critical values. The obtained results may provide some new insight to prevent the computer virus.