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 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 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 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 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 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 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 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 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.     

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.     

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.     

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.     

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.     

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.     

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.     

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 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.     

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 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.