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 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 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.     

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.     

Analysis of a delayed HIV/AIDS epidemic model with saturation incidence

In this paper, a delayed HIV/AIDS epidemic model with saturation incidence is proposed and analyzed. The equilibria and their stability are investigated. The model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. It is found that if the threshold R ₀<1, then the disease-free equilibrium is globally asymptotically stable, and if the threshold R ₀>1, the system is permanent and the endemic equilibrium is asymptotically stable under certain conditions.     

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 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.     

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 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 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 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.     

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.     

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.     

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.     

Modeling diseases with latency and nonlinear incidence rates: global dynamics of a multi‐group model

In this paper, we perform global stability analysis of a multi‐group SEIR epidemic model in which we can consider the heterogeneity of host population and the effects of latency and nonlinear incidence rates. For a simpler version that assumes an identical natural death rate for all groups, and with a gamma distribution for the latency, the basic reproduction number is defined by the theory of the next generation operator and proved to be a sharp threshold determining whether or not disease spread. Under certain assumptions, the disease‐free equilibrium is globally asymptotically stable if R₀≤1 and there exists a unique endemic equilibrium which is globally asymptotically stable if R₀>1. The proofs of global stability of equilibria exploit a matrix‐theoretic method using Perron eigenvetor, a graph‐theoretic method based on Kirchhoff's matrix tree theorem and Lyapunov functionals. Copyright © 2015 John Wiley & Sons, Ltd.     

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.     

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.     

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.     

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.     

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.