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 an SVEIS epidemic model with partial temporary immunity and saturation incidence rate

In this paper, an SVEIS epidemic model for an infectious disease that spreads in the host population through horizontal transmission is investigated. The role that temporary immunity (natural, disease induced, vaccination induced) plays in the spread of disease, is incorporated in the model. The total host population is bounded and the incidence term is of the Holling-type II form. It is shown that the model exhibits two equilibria, namely, the disease-free equilibrium and the endemic equilibrium. The global dynamics are completely determined by the basic reproduction number R₀. If R₀<1, the disease-free equilibrium is globally stable which leads to the eradication of disease from population. If R₀>1, a unique endemic equilibrium exists and is globally stable in the feasible region under certain conditions. Further, the transcritical bifurcation at R₀=1 is explored by projecting the flow onto the extended center manifold. We use the geometric approach for ordinary differential equations which is based on the use of higher-order generalization of Bendixson’s criterion. Further, we obtain the threshold vaccination coverage required to eradicate the disease. Finally, taking biologically relevant parametric values, numerical simulations are performed to illustrate and verify the analytical 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 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 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.     

Dynamics of a delayed epidemic model with non-monotonic incidence rate

A delayed epidemic model with non-monotonic incidence rate which describes the psychological effect of certain serious on the community when the number of infectives is getting larger is studied. The disease-free equilibrium is globally asymptotically stable when R₀<1 and is globally attractive when R₀=1 are derived. On the other hand, The disease is permanent when R₀>1 is also obtained. Numerical simulation results are given to support the theoretical predictions.     

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 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.     

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.     

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.     

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.     

Global analysis of an environmental disease transmission model linking within-host and between-host dynamics

In this paper, a multi-scale mathematical model for environmentally transmitted diseases is proposed which couples the pathogen-immune interaction inside the human body with the disease transmission at the population level. The model is based on the nested approach that incorporates the infection-age-structured immunological dynamics into an epidemiological system structured by the chronological time, the infection age and the vaccination age. We conduct detailed analysis for both the within-host and between-host disease dynamics. Particularly, we derive the basic reproduction number R₀ for the between-host model and prove the uniform persistence of the system. Furthermore, using carefully constructed Lyapunov functions, we establish threshold-type results regarding the global dynamics of the between-host system: the disease-free equilibrium is globally asymptotically stable when R₀ < 1, and the endemic equilibrium is globally asymptotically stable when R₀ > 1. We explore the connection between the within-host and between-host dynamics through both mathematical analysis and numerical simulation. We show that the pathogen load and immune strength at the individual level contribute to the disease transmission and spread at the population level. We also find that, although the between-host transmission risk correlates positively with the within-host pathogen load, there is no simple monotonic relationship between the disease prevalence and the individual pathogen load.     

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.     

Global analysis of an SIS model with an infective vector on complex networks

In this paper, a modified SIS model with an infective vector on complex networks is proposed and analyzed, which incorporates some infectious diseases that are not only transmitted by a vector, but also spread by direct contacts between human beings. We treat direct human contacts as a social network and assume spatially homogeneous mixing between vector and human populations. By mathematical analysis, we obtain the basic reproduction number R₀ and study the effects of various immunization schemes. For the network model, we prove that if R₀<1, the disease-free equilibrium is globally asymptotically stable, otherwise there exists an unique endemic equilibrium such that it is globally attractive. Our theoretical results are confirmed by numerical simulations and suggest a promising way for the control of infectious diseases.     

Two-group SIR epidemic model with stochastic perturbation

A stochastic two-group SIR model is presented in this paper.The existence and uniqueness of its nonnegative solution is obtained,and the solution belongs to a positively invariant set.Furthermore,the globally asymptotical stability of the disease-free equilibrium is deduced by the stochastic Lyapunov functional method if R0 ≤ 1,which means the disease will die out.While if R0 1,we show that the solution is fluctuating around a point which is the endemic equilibrium of the deterministic model in time average.In addition,the intensity of the fluctuation is proportional to the intensity of the white noise.When the white noise is small,we consider the disease will prevail.At last,we illustrate the dynamic behavior of the model and their approximations via a range of numerical experiments.     

Analysis of SE τ IR ω S epidemic disease models with vertical transmission in complex networks

When the role of network topology is taken into consideration, one of the objectives is to understand the possible implications of topological structure on epidemic models. As most real networks can be viewed as complex networks, we propose a new delayed SEτ IRωS epidemic disease model with vertical transmission in complex networks. By using a delayed ODE system, in a small-world (SW) network we prove that, under the condition R0 ≤ 1, the disease-free equilibrium (DFE) is globally stable. When R0 > 1, the endemic equilibrium is unique and the disease is uniformly persistent. We further obtain the condition of local stability of endemic equilibrium for R0 > 1. In a scale-free (SF) network we obtain the condition R1 > 1 under which the system will be of non-zero stationary prevalence.     

Global dynamics of a delayed SIRS epidemic model with a wide class of nonlinear incidence rates

In this paper, by constructing Lyapunov functionals, we consider the global dynamics of an SIRS epidemic model with a wide class of nonlinear incidence rates and distributed delays $\int^{h}_{0} p(\tau)f(S(t),I(t-\tau)) \mathrm{d}\tau$ under the condition that the total population converges to 1. By using a technical lemma which is derived from strong condition of strict monotonicity of functions f(S,I) and f(S,I)/I with respect to S??0 and I>0, we extend the global stability result for an SIR epidemic model if R ₀>1, where R ₀ is the basic reproduction number. By using a limit system of the model, we also show that the disease-free equilibrium is globally asymptotically stable if R ₀=1.     

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.     

On global stability of the intra-host dynamics of malaria and the immune system

In this paper we consider an intra-host model for the dynamics of malaria. The model describes the dynamics of the blood stage malaria parasites and their interaction with host cells, in particular red blood cells (RBC) and immune effectors. We establish the equilibrium points of the system and analyze their stability using the theory of competitive systems, compound matrices and stability of periodic orbits. We established that the disease-free equilibrium is globally stable if and only if the basic reproduction number satisfies R₀?1 and the parasite will be cleared out of the host. If R₀>1, a unique endemic equilibrium is globally stable and the parasites persist at the endemic steady state. In the presence of the immune response, the numerical analysis of the model shows that the endemic equilibrium is unstable.