一类具有阶段结构和分布时滞的种群-传染病模型

讨论了一类具有阶段结构和分布时滞的种群-传染病模型.在模型中,假设染病者没有生育能力.通过分析讨论,得到了地方病平衡点存在的阈值条件及平衡点稳定性和持续生存的充分条件.     

具有阶段结构的SIR传染病模型

研究了一类具有阶段结构的SIR传染病模型，在模型中假设种群分幼年和成年两个阶段，且只有成年种群染病，并且采用与成年易感者数量有关的一般非线性传染率，得到了系统解的有界性及无病平衡点和地方病平衡点存在的条件．通过对平衡点对应的特征方程的讨论得到了平衡点局部渐近稳定的条件，同时证明了平衡点的全局渐近稳定性，并对结论进行了数值模拟．     

染病者有常数输入的传染病模型

讨论在隔离措施下易感者和染病者都有常数移民的传染病模型.给出了模型的地方病平衡点,证明了地方病平衡点的稳定性.     

一类有迁移的SIS流行病模型

研究一类种群有迁移的流行病模型,得到了这类模型的基本再生数R0,证明了R0＜1无病平衡点是局部渐近稳定的,而当R0＞1时无病平衡点是不稳定的.进一步讨论了疾病持续存在与无病平衡点和地方病平衡点全局稳定的条件.     

一类带有一般接触率和常数输入的流行病模型的全局分析

借助极限系统理论和构造适当的Liapunov函数,对带有一般接触率和常数输入的SIR型和SIRS型传染病模型进行讨论．当无染病者输入时,地方病平衡点存在的阈值被找到A·D2对相应的SIR模型,关于无病平衡点和地方病平衡点的全局渐近稳定性均得到充要条件;对相应的SIRS模型,得到无病平衡点和地方病平衡点全局渐近稳定的充分条件．当有染病者输入时,模型不存在无病平衡点．对相应的SIR模型,地方病平衡点是全局渐近稳定的;对相应的SIRS模型,得到地方病平衡点全局渐近稳定的充分条件．     

两类带有确定潜伏期的SEIS传染病模型的分析

通过研究两类带有确定潜伏期的SEIS传染病模型,发现对种群的常数输入和指数输入会使疾病的传播过程产生本质的差异．对于带有常数输入的情形,找到了地方病平衡点存在及局部渐近稳定的阈值,证明了地方病平衡点存在时一定局部渐近稳定,并且疾病一致持续存在．对于带有指数输入的情形,发现地方病平衡点当潜伏期充分小时是局部渐近稳定的,当潜伏期充分大时是不稳定的．     

一类带有非线性传染率的SEIR传染病模型的全局分析

通过假设被传染的易感者一部分经过一段潜伏期后才具有传染性,而另一部分被感染的易感者直接成为传染者,建立了一类带有非线性传染率的SEIR传染病模型,得到了确定疾病是否成为地方病的基本再生数以及无病平衡点和地方病平衡点的全局稳定性.     

一类具有分布时滞和非线性发生率的媒介传染病模型的全局稳定性

建立了一类具有分布时滞和非线性发生率的SIR媒介传染病模型,分析得到了决定疾病是否一致持续存在的基本再生数．而且当基本再生数不大于1时,疾病最终灭绝;当基本再生数大于1时,模型存在惟一的地方病平衡点,并且疾病一致持续存在于种群之中．通过构造Lyapunov泛函,证明了在一定条件下地方病平衡点只要存在就全局稳定．同时指出了证明地方病平衡点全局稳定时可适用的Lyapunov泛函的不惟一性.     

一类具有分布时滞和非线性发生率的媒介传染病模型的全局稳定性

建立了一类具有分布时滞和非线性发生率的ＳＩＲ媒介传染病模型,分析得到了决定疾病是否一致持续存在的基本再生数．而且当基本再生数不大于１时,疾病最终灭绝;当基本再生数大于１时,模型存在惟一的地方病平衡点,并且疾病一致持续存在于种群之中．通过构造Ｌｙａｐｕｎｏｖ泛函,证明了在一定条件下地方病平衡点只要存在就全局稳定．同时指出了证明地方病平衡点全局稳定时可适用的Ｌｙａｐｕｎｏｖ泛函的不惟一性．     

具有常数输入的SEIR模型的稳定性分析

讨论了易感者类和潜伏者类均为常数输入,潜伏期、染病期和恢复期均具有传染力,且传染率为一般传染率的SEIR传染病模型.利用Hurwitz判据证明了地方病平衡点的局部渐近稳定性,进一步利用复合矩阵理论得到了地方病平衡点全局渐近稳定的充分条件.     

Threshold of disease transmission in a patch environment

An epidemic model is proposed to describe the dynamics of disease spread between two patches due to population dispersal. It is proved that reproduction number is a threshold of the uniform persistence and disappearance of the disease. It is found that the dispersal rates of susceptible individuals do not influence the persistence and extinction of the disease. Furthermore, if the disease becomes extinct in each patch when the patches are isolated, the disease remains extinct when the population dispersal occurs; if the disease spreads in each patch when the patches are isolated, the disease remains persistent in two patches when the population dispersal occurs; if the disease disappears in one patch and spreads in the other patch when they are isolated, the disease can spread in all the patches or disappear in all the patches if dispersal rates of infectious individuals are suitably chosen. It is shown that an endemic equilibrium is locally stable if susceptible dispersal occurs and infectious dispersal turns off. If susceptible individuals and infectious individuals have the same dispersal rate in each patch, it is shown that the fractions of infectious individuals converge to a unique endemic equilibrium.     

The effect of population dispersal on the spread of a disease

The effect of population dispersal among n patches on the spread of a disease is investigated. Population dispersal does not destroy the uniqueness of a disease free equilibrium and its attractivity when the basic reproduction number of a disease R₀<1. When R₀>1, the uniqueness and global attractivity of the endemic equilibrium can be obtained if dispersal rates of susceptible individuals and infective individuals are the same or very close in each patch. However, numerical calculations show that population dispersal may result in multiple endemic equilibria and even multi-stable equilibria among patches, and also may result in the extinction of a disease, even though it cannot be eradicated in each isolated patch, provided the basic reproduction numbers of isolated patches are not very large.     

Coexistence in a discrete competition model with dispersal

We propose a discrete-time competition model between two populations to study the effects of dispersal upon population interactions. It is assumed that dispersal occurs after reproduction and in synchrony. We first analyse a two-patch single species population model with no interspecific competition. Based on these results, we derive sufficient conditions for population coexistence. It is proved that the system is uniformly persistent and possesses a unique coexisting equilibrium.     

The role of viral infection in phytoplankton dynamics with the inclusion of incubation class

The role of viral infection in phytoplankton dynamics without and with incubation population class is studied. It is observed that phytoplankton species in the absence of incubated class are unstable around an endemic equilibrium but the presence of delay in the form of incubated class has made it conditionally stable around an endemic equilibrium. We also observe that the dynamical system is very sensitive to the transfer rate from susceptible to incubated class and when it crosses a certain threshold the phytoplankton population start oscillating around the endemic equilibrium, shown both analytically and numerically.     

A model of the dynamic of transmission of malaria, integrating SEIRS, SEIS, SIRS and SIS organization in the host-population

In this paper, we propose and analyse a model of dynamics trans-mission of malaria, incorporating varying degrees p of susceptible and ofinfectious that makes the dynamic of the overall host population integrateSEIRS, SEIS, SIRS and SIS at the same time. For this model we compute anew threshold number and establish the global asymptotic stability of thedisease-free equilibrium when R0 &lt; &lt; 1. If &lt; R0 &lt; 1, the system admits aunique endemic equilibrium (EE) and if R0 &gt; 1 depending on case the systemadmits one or two endemic equilibrium. Numerical simulations are presentedfor dierent value of R0, based on data collected in the literature. Finally,the impact of parameters p and of system dynamics are investigated.     

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.     

QUALITATIVE ANALYSIS OF AN EPIDEMIC MODEL WITH VACCINATION

An SIRS epidemic modei with vaccination, temporary immunity and vary-ing total population size is considered. The threshold of existence of endemic equilibrium is found. The disease-free equilibrium is globally asymptotically stable below the threshold, the endemic equilibrium is globally asymptotically stable above the threshold.     

Approximating the ideal free distribution via reaction-diffusion-advection equations

We consider reaction-diffusion-advection models for spatially distributed populations that have a tendency to disperse up the gradient of fitness, where fitness is defined as a logistic local population growth rate. We show that in temporally constant but spatially varying environments such populations have equilibrium distributions that can approximate those that would be predicted by a version of the ideal free distribution incorporating population dynamics. The modeling approach shows that a dispersal mechanism based on local information about the environment and population density can approximate the ideal free distribution. The analysis suggests that such a dispersal mechanism may sometimes be advantageous because it allows populations to approximately track resource availability. The models are quasilinear parabolic equations with nonlinear boundary conditions.