一类具有Beddington-DeAngelis型功能反应函数的HIV病毒动力学系统模型的稳定性

基于Nowak等于1996年提出的一类经典的HIV病毒动力学模型,考虑了一类具有Beddington-DeAngelis功能反映函数的HIV病毒动力学模型,并研究了无病毒平衡点的全局稳定性与感染平衡点的局部稳定性等.     

一类具有病毒饱和增殖的病毒-免疫动力学模型的分析

在假设病毒增殖率为Michaelis-Menten函数的基础上,提出了一类病毒增殖具有饱和性的病毒与特异性免疫细胞相互作用的模型.分析发现该模型至多有两个正平衡点并会发生鞍结点分支;借助中心流形定理讨论了平衡点的局部稳定性;运用Bendixson-Dulac定理排除了周期解的存在性,进而得到模型的全局动力学性态.数值模拟显示了病毒与免疫系统相互作用的结果对初始状态的依赖性,以及在作用过程中会出现病毒载量和免疫细胞种群数量的持续振荡.     

复杂网络上的病毒免疫策略研究

为了给预防病毒传播提供指导意见并且更好地对病毒传播行为进行预测和控制,主要研究了几种经典复杂网络中病毒传播的模型,并对几种复杂网络病毒免疫的模型特点进行了分析,通过对这些病毒免疫模型在多局域加权网络中应用不足的分析,对多局域加权网络的病毒免疫策略进行了相应的研究.     

一类具有时滞的SIRS传染病模型的Hopf分岔分析

研究了一类具有时滞的SIRS传染病模型.首先,利用特征值理论得到了模型的有病毒平衡点,然后通过分析在有病毒平衡点处的相应特征方程根的分布,得到有病毒平衡点处的局部渐近稳定和发生Hopf分岔的时滞临界点.以时滞为分岔参数,研究了SIRS传染病模型存在Hopf分岔的条件.     

一类具有双线性传染率的HIV/AIDS病毒动力学改进模型

针对HIV/AIDS传播的具有常数移民和指数出生的SI型模型,为了更加符合实际意义,对具有双线性传染率的模型进行局部改进,并对改进后的动力学模型进行了简化.对于改进后的模型,证明了平衡点的存在与局部稳定性,并证明了传染病毒的灭绝与持续性,得到了传染病毒的基本再生数.结果表明:当单位时间内从外界迁入人口中染病者的比例系数c近似等于零时,基本再生数小于1时,传染病毒最终灭绝;当基本再生数大于1时,模型存在唯一的正平衡点,且是局部渐近稳定的,说明传染病毒一致持续存在.     

带有免疫反应的病毒动力学模型的全局稳定性

利用Lyapunov函数研究了带有免疫反应的病毒动力学模型的全局稳定性.当基本再生数R0≤1时.病毒在体内清除;当R0>1时,病毒在体内持续生存.并且模型的正解当免疫再生数R1≤1时,趋于无免疫平衡点,当R1>1.趋于地方病平衡点.     

具斑块迁移的病毒模型的稳定性分析

研究了一类未感染细胞斑在两斑块间迁移的病毒模型.获得了无病平衡点全局稳定性以及地方病平衡点稳定性的充分条件.研究结果表明阈值R <1且感染细胞生成病毒的速度相对小而病毒细胞死亡率足够大时,病毒趋于灭绝;而阈值R> 1且感染细胞生成病毒的速度相对大而病毒细胞死亡率足够小时,病毒持续流行.     

一类HIV病毒动力学模型的全局稳定性与周期解

建立了一类较广泛的HIV感染CD4+T细胞病毒动力学模型,给出了一个感染细胞在其整个感染期内产生的病毒的平均数(基本再生数)R0的表达式,运用Lyapunov原理和Routh-Hurwitz判据得到了该模型的未感染平衡点与感染平衡点的存在性与稳定性条件.同时也得到了模型存在轨道渐近稳定周期解和系统持续生存的条件,并通过数值模拟验证了所得到的结果.     

一类具有扩散和Beddington-DeAngelis反应函数的病毒模型的全局稳定性

研究了一类具有扩散和Beddington-DeAngelis反应函数的病毒模型.通过构造Lyapunov函数,证明了模型的感染平衡点是全局渐近稳定的.     

具有垂直传染和接触传染的传染病模型的稳定性研究

本文研究了一类具有垂直传染和接触传染的传染病模型.利用常微分方程定性与稳定性方法,分析了该模型非负平衡点的存在性及其局部稳定性.同时,利用LaSalle不变性原理和通过构造适当的Lyapunov函数,获得了平凡平衡点、无病平衡点和地方病平衡点全局渐近稳定的充分条件.结果表明当基本再生数小于等于1时,所有种群趋于灭绝;当基本再生数大于1和病毒主导再生数小于1时,病毒很快被清除;当基本再生数大于1和病毒主导再生数大于1以及满足一定条件时,病毒持续流行并将成为一种地方病.     

A with-in host Dengue infection model with immune response

A model of viral infection of monocytes population by Dengue virus is formulated here. The model can capture phenomena that dengue virus is quickly cleared in approximately 7 days after the onset of the symptoms. The model takes into account the immune response. It is shown that the quantity of free virus is decreasing when the viral invasion rate is increasing. The basic reproduction ratio of model without immune response is reduced significantly by adding the immune response. Numerical simulations indicate that the growth of immune response and the invasion rate are very crucial in identification of the intensity of infection.     

Birth-pulse models of Wolbachia-induced cytoplasmic incompatibility in mosquitoes for dengue virus control

Dengue fever, which affects more than 50 million people a year, is the most important arboviral disease in tropical countries. Mosquitoes are the principal vectors of the dengue virus but some endosymbiotic Wolbachia bacteria can stop the mosquitoes from reproducing and so interrupt virus transmission. A birth-pulse model of the spread of Wolbachia through a population of mosquitoes, incorporating the effects of cytoplasmic incompatibility (CI) and different density dependent death rate functions, is proposed. Strategies for either eradicating mosquitoes or using population replacement by substituting uninfected mosquitoes with infected ones for dengue virus prevention were modeled. A model with a strong density dependent death function shows that population replacement can be realized if the initial ratio of number of infected to the total number of mosquitoes exceeds a critical value, especially when transmission from mother to offspring is perfect. However, with a weak density dependent death function, population eradication becomes difficult as the system’s solutions are sensitive to initial values. Using numerical methods, it was shown that population eradication may be achieved regardless of the infection ratio only when parameters lie in particular regions and the initial density of uninfected is low enough.     

An epidemic model to evaluate the homogeneous mixing assumption

Many epidemic models are written in terms of ordinary differential equations (ODE). This approach relies on the homogeneous mixing assumption; that is, the topological structure of the contact network established by the individuals of the host population is not relevant to predict the spread of a pathogen in this population. Here, we propose an epidemic model based on ODE to study the propagation of contagious diseases conferring no immunity. The state variables of this model are the percentages of susceptible individuals, infectious individuals and empty space. We show that this dynamical system can experience transcritical and Hopf bifurcations. Then, we employ this model to evaluate the validity of the homogeneous mixing assumption by using real data related to the transmission of gonorrhea, hepatitis C virus, human immunodeficiency virus, and obesity.     

A stochastic model for internal HIV dynamics

In this paper we analyse a stochastic model representing HIV internal virus dynamics. The stochasticity in the model is introduced by parameter perturbation which is a standard technique in stochastic population modelling. We show that the model established in this paper possesses non-negative solutions as this is essential in any population dynamics model. We also carry out analysis on the asymptotic behaviour of the model. We approximate one of the variables by a mean reverting process and find out the mean and variance of this process. Numerical simulations conclude the paper.     

基于两斑块和人口流动的SIR传染病模型的稳定性

根据传染病动力学原理,考虑人口在两斑块上流动且具有非线性传染率,建立了一类基于两斑块和人口流动的SIR传染病模型.利用常微分方程定性与稳定性方法,分析了模型永久持续性和非负平衡点的存在性,通过构造适当的Lyapunov函数和极限系统理论,获得无病平衡点和地方病平衡点全局渐近稳定的充分条件.研究结果表明:基本再生数是决定疾病流行与否的阈值,当基本再生数小于等于1时,感染者逐渐消失,病毒趋于灭绝;当基本再生数大于1并满足永久持续条件时,感染者持续存在且病毒持续流行并将成为一种地方病.     

Dynamics of a two-strain vaccination model for polio

A new deterministic model for the transmission dynamics of two strains of polio, the vaccine-derived polio virus (VDPV) and the wild polio virus (WPV), in a population is designed and rigorously analysed. It is shown that Oral Polio Vaccine (OPV) reversion (leading to increased incidences of WPV and VDPV strains), together with the combined effect of vaccinating a fraction of the unvaccinated susceptible and missed susceptible children, could induce the phenomenon of backward bifurcation when the associated reproduction number of the model is less than unity. Furthermore, the model undergoes competitive exclusion, where the strain with the higher reproduction number (greater than unity) drives the other (with reproduction number less than unity) to extinction. In the absence of OPV reversions (leading to the co-existence of both strains in the population), it is shown that the disease-free equilibrium of the model is globally-asymptotically stable whenever the associated reproduction number is less than unity. Numerical simulations of the model suggest that the model undergoes the phenomenon of competitive exclusion, where the strain with the higher reproduction number (greater than unity) drives the other to extinction. Furthermore, co-existence of the two strains is feasible if their respective reproduction number are equal or approximately equal (and greater than unity).     

Evolving phylogenies of trait-dependent branching with mutation and competition,Part I: Existence

We propose a type-dependent branching model with mutation and competition for modelling phylogenies of a virus population. The competition kernel depends on the total mass, the types of the virus particles, and the genetic information available through the number of nucleotide substitutions separating the virus particles. We consider evolving phylogenies in the huge population, short reproduction time and frequent mutation regime, show tightness in the space of marked metric measure spaces and characterize the limit through a martingale problem. Due to heterogeneity in the branching rates, the phylogenies are not ultra-metric. We therefore develop new techniques for verifying compact containment.     

Dynamics of a virus–host model with an intrinsic quota

In this work we develop and analyze a mathematical model describing the dynamics of infection by a virus of a host population in a freshwater environment. Our model, which consists of a system of nonlinear ordinary differential equations, includes an intrinsic quota, that is, we use a nutrient (e.g., phosphorus) as a limiting element for the host and potentially for the virus. Motivation for such a model arises from studies that raise the possibility that on the one hand, viruses may be limited by phosphorus (Bratbak et al. [17]), and on the other, that they may have a role in stimulating the host to acquire the nutrient (Wilson [18]). We perform an in-depth mathematical analysis of the system including the existence and uniqueness of solutions, equilibria, asymptotic, and persistence analysis. We compare the model with experimental data, and find that biologically meaningful parameter values provide a good fit. We conclude that the mathematical model supports the hypothesized role of stored nutrient regulating the dynamics, and that the coexistence of virus and host is the natural state of the system.     

具有扩散病毒感染群体动力学模型的稳定性与Hopf分歧

讨论了一个具有诺依曼边界条件扩散病毒感染群体动力学模型.证明了模型正常数平衡点的稳定性和扩散引起的Hopf分歧的存在性.