Disease-induced mortality in density-dependent discrete-time S-I-S epidemic models

The dynamics of simple discrete-time epidemic models without disease-induced mortality are typically characterized by global transcritical bifurcation. We prove that in corresponding models with disease-induced mortality a tiny number of infectious individuals can drive an otherwise persistent population to extinction. Our model with disease-induced mortality supports multiple attractors. In addition, we use a Ricker recruitment function in an SIS model and obtained a three component discrete Hopf (Neimark-Sacker) cycle attractor coexisting with a fixed point attractor. The basin boundaries of the coexisting attractors are fractal in nature, and the example exhibits sensitive dependence of the long-term disease dynamics on initial conditions. Furthermore, we show that in contrast to corresponding models without disease-induced mortality, the disease-free state dynamics do not drive the disease dynamics.     

Global Properties of Infectious Disease Models with Nonlinear Incidence

We consider global properties for the classical SIR, SIRS and SEIR models of infectious diseases, including the models with the vertical transmission, assuming that the horizontal transmission is governed by an unspecified function f(S,I). We construct Lyapunov functions which enable us to find biologically realistic conditions sufficient to ensure existence and uniqueness of a globally asymptotically stable equilibrium state. This state can be either endemic, or infection-free, depending on the value of the basic reproduction number.     

Global Stability of Equilibria in a Two-Sex HPV Vaccination Model

Human papillomavirus (HPV) is the primary cause of cervical carcinoma and its precursor lesions, and is associated with a variety of other cancers and diseases. A prophylactic quadrivalent vaccine against oncogenic HPV 16/18 and warts-causing genital HPV 6/11 types is currently available in several countries. Licensure of a bivalent vaccine against oncogenic HPV 16/18 is expected in the near future. This paper presents a two-sex, deterministic model for assessing the potential impact of a prophylactic HPV vaccine with several properties. The model is based on the susceptible-infective-removed (SIR) compartmental structure. Important epidemiological thresholds such as the basic and effective reproduction numbers and a measure of vaccine impact are derived. We find that if the effective reproduction number is greater than unity, there is a locally unstable infection-free equilibrium and a unique, globally asymptotically stable endemic equilibrium. If the effective reproduction number is less than unity, the infection-free equilibrium is globally asymptotically stable, and HPV will be eliminated.     

Infection-age structured epidemic models with behavior change or treatment

We formulate infection-age structured susceptible-infective-removed (SIR) models with behavior change or treatment of infections. Individuals change their behavior or have treatment after they are infected. Using infection age as a continuous variable, and dividing infectives into discrete groups with different infection stages, respectively, we formulate a partial differential equation model and an ordinary differential equation model with behavior change or treatment. We derive explicit formulas for the reproductive number by linear stability analysis of the infection-free equilibrium, and explicit formulas for the unique endemic equilibrium, when it exists, for both models. These formulas provide mathematical theoretical frameworks for analysis of impact of behavior change or treatment of infection to the transmission dynamics of infectious diseases. We study several special cases and provide sensitivity analysis for the reproductive numbers with respect to model parameters based on those formulas.     

Infection-age structured epidemic models with behavior change or treatment

We formulate infection-age structured susceptible-infective-removed (SIR) models with behavior change or treatment of infections. Individuals change their behavior or have treatment after they are infected. Using infection age as a continuous variable, and dividing infectives into discrete groups with different infection stages, respectively, we formulate a partial differential equation model and an ordinary differential equation model with behavior change or treatment. We derive explicit formulas for the reproductive number by linear stability analysis of the infection-free equilibrium, and explicit formulas for the unique endemic equilibrium, when it exists, for both models. These formulas provide mathematical theoretical frameworks for analysis of impact of behavior change or treatment of infection to the transmission dynamics of infectious diseases. We study several special cases and provide sensitivity analysis for the reproductive numbers with respect to model parameters based on those formulas.     

Dynamics of malaria transmission model with sterile mosquitoes

In this paper, a malaria transmission model with sterile mosquitoes is considered. We first formulate a simple SEIR malaria transmission model as our baseline model. Then sterile mosquitoes are introduced into the baseline model. We consider the case that the release rate of sterile mosquitoes is proportional to the wild mosquito population size. To investigate the impact of releasing sterile mosquitoes on the malaria transmission, the dynamics of the baseline model and the models with the sterile mosquitoes are discussed. We derive formulas of the reproductive numbers and explore the existence of endemic equilibrium as the reproductive number is more than unity for these models. It is shown that both the baseline model and the models with the sterile mosquitoes undergo backward bifurcations. Based on theoretical analysis and numerical simulation, we investigate the impact of releasing sterile mosquitoes on malaria transmission.     

Global Properties of <Emphasis Type="Italic">SIR</Emphasis> and <Emphasis Type="Italic">SEIR</Emphasis> Epidemic Models with Multiple Parallel Infectious Stages

We consider global properties of compartment SIR and SEIR models of infectious diseases, where there are several parallel infective stages. For instance, such a situation may arise if a fraction of the infected are detected and treated, while the rest of the infected remains undetected and untreated. We assume that the horizontal transmission is governed by the standard bilinear incidence rate. The direct Lyapunov method enables us to prove that the considered models are globally stable: There is always a globally asymptotically stable equilibrium state. Depending on the value of the basic reproduction number R ₀, this state can be either endemic (R ₀>1), or infection-free (R ₀≤1).     

一类具有垂直传染和预防接种的传染病模型的稳定性

考虑了垂直传染和预防接种因素对传染病流行影响的SEIRS模型,主要研究了系统的平衡点及其稳定性,得出当预防接种水平超过某一个阈值时疾病可以根除,若接种水平低于阈值时疾病将流行.     

改进的病毒感染动力学模型的稳定性分析

提出一个改进的乙肝病毒感染动力学模型.本模型有三个平衡点.对于HBV感染人群,三个平衡点分别对应于三类人群：感染病毒后自愈人群、健康带毒人群、慢性乙肝患者人群.证明了当模型导出的基本复制数R_0〈1时病毒清除平衡点具有局部稳定性和全局渐近稳定性,当1〈R_0〈k_3d/（k_2λ-k_3a）＋1时持续带毒平衡点具有局部稳定性.     

Global Dynamics of an In-host Viral Model with Intracellular Delay

The dynamics of a general in-host model with intracellular delay is studied. The model can describe in vivo infections of HIV-I, HCV, and HBV. It can also be considered as a model for HTLV-I infection. We derive the basic reproduction number R ₀ for the viral infection, and establish that the global dynamics are completely determined by the values of R ₀. If R ₀≤1, the infection-free equilibrium is globally asymptotically stable, and the virus are cleared. If R ₀>1, then the infection persists and the chronic-infection equilibrium is locally asymptotically stable. Furthermore, using the method of Lyapunov functional, we prove that the chronic-infection equilibrium is globally asymptotically stable when R ₀>1. Our results shows that for intercellular delays to generate sustained oscillations in in-host models it is necessary have a logistic mitosis term in target-cell compartments.     

Existence, multiplicity and stability of endemic states for an age-structured S-I epidemic model

We study an S-I type epidemic model in an age-structured population, with mortality due to the disease. A threshold quantity is found that controls the stability of the disease-free equilibrium and guarantees the existence of an endemic equilibrium. We obtain conditions on the age-dependence of the susceptibility to infection that imply the uniqueness of the endemic equilibrium. An example with two endemic equilibria is shown. Finally, we analyse numerically how the stability of the endemic equilibrium is affected by the extra-mortality and by the possible periodicities induced by the demographic age-structure.     

On the role of long incubation periods in the dynamics of acquired immunodeficiency syndrome (AIDS)

In this study, we investigate systematically the role played by the reproductive number (the number of secondary infections generated by an infectious individual in a population of susceptibles) on single group populations models of the spread of HIV/AIDS. Our results for a single group model show that if R 1, the disease will die out, and strongly suggest that if R > 1 the disease will persist regardless of initial conditions. Our extensive (but incomplete) mathematical analysis and the numerical simulations of various research groups support the conclusion that the reproductive number R is a global bifurcation parameter. The bifurcation that takes place as R is varied is a transcritical bifurcation; in other words, when R crosses 1 there is a global transfer of stability from the infection-free state to the endemic equilibrium, and vice versa. These results do not depend on the distribution of times spent in the infectious categories (the survivorship functions). Furthermore, by keeping all the key statistics fixed, we can compare two extremes: exponential survivorship versus piecewise constant survivorship (individuals remain infectious for a fixed length of time). By choosing some realistic parameters we can see (at least in these cases) that the reproductive numbers corresponding to these two extreme cases do not differ significantly whenever the two distributions have the same mean. At any rate a formula is provided that allows us to estimate the role played by the survivorship function (and hence the incubation period) in the global dynamics of HIV. These results support the conclusion that single population models of this type are robust and hence are good building blocks for the construction of multiple group models. Our understanding of the dynamics of HIV in the context of mathematical models for multiple groups is critical to our understanding of the dynamics of HIV in a highly heterogeneous population.     

Effect of a sharp change of the incidence function on the dynamics of a simple disease

We investigate two cases of a sharp change of incidencec functions on the dynamics of a susceptible-infective-susceptible epidemic model. In the first case, low population levels have mass action incidence, while high population levels have proportional incidence, the switch occurring when the total population reaches a certain threshold. Using a modified Dulac theorem, we prove that this system has a single equilibrium which attracts all solutions for which the disease is present and the population remains bounded. In the second case, an increase of the number of infectives leads to a mass action term being added to a standard incidence term. We show that this allows a Hopf bifurcation to occur, with periodic orbits being generated when a locally asymptotically stable equilibrium loses stability.     

一类带有非线性感染率传染病模型的动力学性质（英文）

主要介绍了一类带有非线性感染率的传染病模型.并且证明了当基本再生数Ro≤1时,无病平衡点是全局稳定的,当基本再生数R_0〉1时,疾病持续.     

Rational behavioral response and the transmission of STDs

The susceptible-infected (SI) model is extended by allowing for individual optimal choices of self-protective actions against infection, where agents differ with respect to preferences and costs of self-protection. It is shown that a unique endemic equilibrium prevalence exists when the basic reproductive number of a STD is strictly greater than unity, and that the disease-free equilibrium is the unique steady state equilibrium when the basic reproductive number is less than or equal to one. Unlike in models that take individual behavior as given and fixed, the endemic equilibrium prevalence need not vary monotonically with respect to the basic reproductive number. Specifically, with endogenously determined self-protective behavior, a reduction in the basic reproductive number may in fact increase the endemic equilibrium prevalence. The global stability of the endemic steady state is established for the case of a homogeneous population by showing that, for any non-zero initial disease prevalence, there exists an equilibrium path which converges to the endemic steady state.     

Global dynamics of a staged-progression model with amelioration for infectious diseases

We analyze the global dynamics of a mathematical model for infectious diseases that progress through distinct stages within infected hosts with possibility of amelioration. An example of such diseases is HIV/AIDS that progresses through several stages with varying degrees of infectivity; amelioration can result from a host's immune action or more commonly from antiretroviral therapies, such as highly active antiretroviral therapy. For a general n-stage model with constant recruitment and bilinear incidence that incorporates amelioration, we prove that the global dynamics are completely determined by the basic reproduction number R(0). If R(0)≤1, then the disease-free equilibrium P(0) is globally asymptotically stable, and the disease always dies out. If R(0)>1, P(0) is unstable, a unique endemic equilibrium P* is globally asymptotically stable, and the disease persists at the endemic equilibrium. Impacts of amelioration on the basic reproduction number are also investigated.     

Linking immunological and epidemiological dynamics of HIV: the case of super-infection

In this paper, a two-strain model that links immunological and epidemiological dynamics across scales is formulated. On the within-host scale, the two strains eliminate each other with the strain with the larger immunological reproduction persisting. However, on the population scale superinfection is possible, with the strain with larger immunological reproduction number super-infecting the strain with the smaller immunological reproduction number. The two models are linked through the age-since-infection structure of the epidemiological variables. In addition, the between-host transmission and the disease-induced death rate depend on the within-host viral load. The immunological reproduction numbers, the epidemiological reproduction numbers and invasion reproduction numbers are computed. Besides the disease-free equilibrium, there are two population-level strain one and strain two isolated equilibria, as well as a population-level coexistence equilibrium when both invasion reproduction numbers are greater than one. The single-strain population-level equilibria are locally asymptotically stable suggesting that in the absence of superinfection oscillations do not occur, a result contrasting previous studies of HIV age-since-infection structured models. Simulations suggest that the epidemiological reproduction number and HIV population prevalence are monotone functions of the within-host parameters with reciprocal trends. In particular, HIV medications that decrease within-host viral load also increase overall population prevalence. The effect of the immunological parameters on the population reproduction number and prevalence is more pronounced when the initial viral load is lower.     

具有饱和发生率的病毒感染模型的全局稳定性分析

讨论了一类具有饱和发生率的病毒感染数学模型,分析得到了无病平衡点和持续带毒平衡点的全局稳定性条件.当病毒感染的基本再生数R_01时,无病平衡点全局渐近稳定;当R_01时,持续带毒平衡点全局渐近稳定.     

The Ross-Macdonald model in a patchy environment

We generalize to n patches the Ross-Macdonald model which describes the dynamics of malaria. We incorporate in our model the fact that some patches can be vector free. We assume that the hosts can migrate between patches, but not the vectors. The susceptible and infectious individuals have the same dispersal rate. We compute the basic reproduction ratio R(0). We prove that if R(0)1, then the disease-free equilibrium is globally asymptotically stable. When R(0)>1, we prove that there exists a unique endemic equilibrium, which is globally asymptotically stable on the biological domain minus the disease-free equilibrium.     

A simple mathematical model for Ebola in Africa

We deal with the following question: Can the consumption of contaminated bush meat, the funeral practices and the environmental contamination explain the recurrence and persistence of Ebola virus disease outbreaks in Africa? We develop an SIR-type model which, incorporates both the direct and indirect transmissions in such a manner that there is a provision of Ebola viruses. We prove that the full model has one (endemic) equilibrium which is locally asymptotically stable whereas, it is globally asymptotically stable in the absence of the Ebola virus shedding in the environment. For the sub-model without the provision of Ebola viruses, the disease dies out or stabilizes globally at an endemic equilibrium. At the endemic level, the number of infectious is larger for the full model than for the sub-model without provision of Ebola viruses. We design a nonstandard finite difference scheme, which preserves the dynamics of the model. Numerical simulations are provided.