一类带有扩散和B-D反应项的病毒模型的稳定性分析

本文研究了齐次Neumann边界条件下带有扩散和B-D反应项病毒模型的平衡解渐近稳定性.利用弱耦合抛物不等式组的最大值原理,给出了模型解的先验估计.利用赫尔维茨(Hurwitz)定理,分析了平衡解的局部渐近稳定性.结果表明:当基本再生数大于1时,地方病平衡态局部渐近稳定;当基本再生数小于1时,无病平衡态局部渐近稳定.同时,利用构造上下解及其单调迭代序列的方法证明了无病平衡解的全局渐近稳定性,该结果表明:当控制细胞生成率或者感染率或者感染细胞裂解率充分小时,无病平衡解的全局渐近稳定.     

具有时滞和旅途过程中有传染的两斑块SIS模型的全局动力学

本文建立了一个具有时滞的SI S模型,研究了旅途过程中疾病的传染.得到了基本再生数.通过线性化方法和比较原理,证明了当基本再生数小于1时无病平衡点是全局渐近稳定的,疾病绝灭.当基本再生数大于1时,系统存在唯一的全局吸引的地方病平衡点,且疾病持续生存.数值模拟验证了扩散率对疾病传播的影响.分析了基本再生数对扩散率的依赖性.     

具有时滞和旅途过程中有传染的两斑块SIS模型的全局动力学（英文）

本文建立了一个具有时滞的SI S模型,研究了旅途过程中疾病的传染.得到了基本再生数.通过线性化方法和比较原理,证明了当基本再生数小于1时无病平衡点是全局渐近稳定的,疾病绝灭.当基本再生数大于1时,系统存在唯一的全局吸引的地方病平衡点,且疾病持续生存.数值模拟验证了扩散率对疾病传播的影响.分析了基本再生数对扩散率的依赖性.     

具有一般形式非线性饱和传染率染病年龄结构SIS模型渐近分析

：研究一类具有一般形式非线性饱和传染率染病年龄结构SIS流行病传播数学模型动力学性态,得到疾病绝灭和持续生存的阈值条件——基本再生数。当基本再生数小于或等于1时,仅存在无病平衡点,且在其小于1的情况下,无病平衡点全局渐遗稳定,疾病将逐渐消除;当基本再生数大于1时,存在不稳定的无病平衡点和唯一的局部渐近稳定的地方病平衡点,疾病将持续存在。已有的两类模型可视为本模型的特例,其相关结论可作为本文的推论。     

具有预防接种的非线性传染率传染病模型的稳定性

本文讨论了一个采取预防接种措施的非线性传染率传染病模型,得到了决定疾病流行与否的阈值θ,当θ>1时,仅存在无病平衡点E0,是渐近稳定的,当θ<1时,存在两个平衡点:无病平衡点E0和地方病平衡点E ,其中无病平衡点E0不稳定。在不考虑免疫的丧失或者不考虑因病死亡的因素的情况下,当θ>1时E0全局渐近稳定;当θ<1时E 全局渐近稳定。     

一类非标准离散霍乱动力学模型

本文旨在利用非标准有限差分方法离散并求解一个包含预防接种的霍乱传染病模型．该离散模型具有和对应的原连续模型一致的平衡点,正性和有界性等性质．其次本文证明当基本再生数小于 1 时,无病平衡点是局部渐近稳定和全局渐近稳定的;当基本再生数大于 1 时,通过构造适当的 Lyapunov 函数,地方病平衡点也是全局渐近稳定的．最后利用离散模型可以成功模拟 2008 年津巴布韦霍乱,并可数值证明离散模型的稳定性,且与步长和初始条件等无关,再与其他离散方法比较验证 NSFD 方法的优势所在．     

一类具有非线性发生率的SEIR传染病模型的全局稳定性分析

本文对一类具有非线性发生率的SEIR传染病模型进行了研究.确定了决定疾病灭绝或持续存在的阈值-基本再生数,并分析了模型的平衡点的存在性;通过构造恰当的Lyapunov函数,运用La Salle不变性原理证明了当基本再生数小于或等于1时,无病平衡点是全局渐进稳定的;利用Lyapunov直接方法证明了当基本再生数大于1时,地方病平衡点是全局渐进稳定的.最后,将发生率具体化用数值模拟验证了所得理论分析结果的正确性.     

非线性高维自治微分系统 SEIQR 流行病模型全局稳定性

研究具有隔离仓室及饱和接触率的非线性高维自治微分系统SEIQR流行病传播数学模型,得到疾病绝灭与否的阈值一基本再生数R_0,证明了无病平衡点和地方病平衡点的存在性及全局渐近稳定性,揭示了隔离对疾病控制的积极作用,推广了已有的研究结果。     

一类带接种和年龄结构的流行病模型分析

讨论了一类具有年龄结构和接种措施的SEIB流行病模型，其中治愈者无终生免疫力。获得了再生数的解析表示，无病平衡态的局部稳定性及在一定条件下的全局稳定性。证明了地方病平衡态的存在性和不存在性。     

具有年龄结构的流行病模型的全局稳定性北大核心CSCD

基于重新感染情形,建立了一个具有接种、潜伏和染病年龄结构的流行病模型,目的在于讨论疫苗接种年龄、潜伏年龄和感染年龄对模型全局动力学的影响,得到了模型的全局动力学由基本再生数决定。首先,利用偏微分方程沿特征线积分理论,给出了模型解的存在唯一性、连续有界性和渐近光滑性;其次,利用微分方程解的理论,得到模型的平衡点和基本再生数。再次,结合引入的基本再生数和构造的Lyapunov函数,应用LaSalle不变性原理得到结论:若基本再生数小于1,则无病平衡点全局渐近稳定;若基本再生数大于1,则无病平衡点不稳定。最后,数值模拟验证了所讨论模型的解收敛于无病平衡点。     

一类含多时滞和扩散项的非标准离散模型

建立了一类以媒体效应作为主要预防传染病传播手段、并且含有多时滞和扩散项的传染病连续模型,并证明了该连续模型平衡点的全局稳定性。其次,利用非标准有限差分方法对该连续模型进行离散,离散后的模型具有和原连续模型一致的动力学性质。通过构造适当的李雅普诺夫函数,证明离散模型的平衡点在一定条件下也都是全局渐近稳定的。最后,数值模拟验证了理论结果。     

Spread of disease involving time delay and population dispersal

An epidemic model with time delay is proposed to incorporate population dispersal between patches, where time delay arises very naturally. We establish a threshold above which the disease is uniformly persistent. Sufficient conditions that lead to the extinction of the disease are obtained. We give sufficient condition for the existence of the positive equilibrium. We also show that when the positive equilibrium exists, it is globally asymptotically stable. Some examples are given to illustrate the effect of population dispersal, time delay and dispersal-related mortality. It is found that a disease may spread when the population migrates in two patches, even though it dies out in some isolated patches. It is also found that population dispersal can reduce the disease spread for strong dispersal rate, large time delay and dispersal-related mortality.     

Global stability of infection‐free state and endemic infection state of a modified human immunodeficiency virus infection model

This study proposes a modified human immunodeficiency virus (HIV) infection differential equation model with a saturated infection rate. This model has an infection‐free equilibrium point and an endemic infection equilibrium point. Using Lyapunov functions and LaSalle’s invariance principle shows that if the model’s basic reproductive number R ₀ < 1, the infection‐free equilibrium point is globally asymptotically stable, otherwise the endemic infection equilibrium point is globally asymptotically stable. It is shown that a forward bifurcation will occur when R ₀ = 1. The basic reproductive number R ₀ of the modified model is independent of plasma total CD4⁺ T cell counts and thus the modified model is more reasonable than the original model proposed by Buonomo and Vargas‐De‐León. Based on the clinical data from HIV drug resistance database of Stanford University, using the proposed model simulates the dynamics of two group patients’ anti‐HIV infection treatments. The simulation results have shown that the first 4 weeks’ treatments made the two group patients’ R′ ₀ < 1, respectively. After the period, drug resistance made the two group patients’ R′ ₀ > 1. The results explain why the two group patients’ mean CD4⁺ T cell counts raised and mean HIV RNA levels declined in the first period, but contrary in the following weeks.Inspec keywords: microorganisms, cellular biophysics, differential equations, Lyapunov methods, blood, drugs, patient treatment, RNAOther keywords: global stability, infection‐free state, endemic infection state, modified human immunodeficiency virus infection model, HIV, differential equation model, saturated infection rate, infection‐free equilibrium point, endemic infection equilibrium point, Lyapunov functions, LaSalle invariance principle, forward bifurcation, plasma total CD4⁺ T cell counts, HIV drug resistance database, mean HIV RNA levels     

Analysis and simulation of an Adefovir anti‐hepatitis B virus infection therapy immune model with alanine aminotransferase

Hepatitis B virus (HBV) infection models and anti‐HBV infection therapy models have been set up to understand and explain clinical phenomena. Many of these models have been proposed based on Zeuzem et al. and Nowak et al.''s basic virus infection model (BVIM). Some references have pointed out that the basic infection reproductive number of the BVIM is biologically questionable and gave the modified models with standard mass action incidences. This study describes one anti‐HBV therapy immune model with alanine aminotransferase (ALT) based on standard mass action incidences. There are two basic infection reproductive numbers R ₀ and R ₁ in the model. It is proved that if R ₀ < 1 and R ₁ < 1, the disease free equilibrium is locally and globally asymptotically stable, respectively. For the endemic equilibrium, simulation shows that if R ₁ > 1, it may be also globally asymptotically stable. Simulations based on clinical data of HBV DNA and ALT can explain some clinical phenomena. Simulations of the correlation between liver cells, HBV DNA, cytotoxic T lymphocytes and ALT are also given.Inspec keywords: blood, cellular biophysics, diseases, DNA, enzymes, liver, microorganisms, molecular biophysics, patient treatmentOther keywords: Adefovir antihepatitis B virus infection therapy immune model analysis, Adefovir antihepatitis B virus infection therapy immune model simulation, alanine aminotransferase, clinical phenomena, basic infection reproductive number, standard mass action incidences, disease free equilibrium, asymptotic stability, endemic equilibrium, HBV DNA, ALT, liver cells, cytotoxic T lymphocytes     

一个具有暂时免疫和非线性接触率的SIS流行病模型的分析

本文研究一个具有时滞,一般接触率,常数出生和疾病引起死亡的流行病模型.假设时滞表示暂时免疫期,即恢复者再次变成易感者所需要的时间,同时在模型中考虑了对易感者和恢复者的接种.本文得到了基本再生数R0.分析了模型的无病平衡点和地方病平衡点的存在性.通过Hurwitz准则,研究了无病平衡点和地方病平衡点的局部渐近稳定性.通过Liapunov泛函和Lasalle不变原理,证明了无病平衡点的全局渐近稳定性及在双线性接触率的情况下地方病平衡点的全局渐近稳定性.研究结果表明:R0与对易感者的有效接种率P有关,并且通过增加接种率P可以根除疾病.最后给出了数值模拟.     

带常数输入率TB模型的全局稳定性

研究了各分类均具有常数输入率先的一个TB模型的全局稳定性。根据广义的Bendixson判据，证明了当输入中含有受感染者时，模型不存在无病平衡点而具有唯一的地方病平衡点。当感染者的治愈率较小时，证明了该平衡点的全局渐近稳定性。     

Global dynamics of a time delayed SIR model with varying population size

A disease transmission model of susceptible-infective-recovered type with a constant latent period is analysed. The global dynamics of the disease-free equilibrium is investigated. If the basic reproduction number is greater than unity, a unique endemic equilibrium exists. Using Lyapunov functional approach, this endemic equilibrium is globally stable in the feasible region. The disease will persist (and is permanent) at the endemic equilibrium if it is initially present. The effects of loss of immunity on the dynamics of the model are analysed, and the parameters that drive the disease dynamics are obtained. Numerical simulations support our analytical results and illustrate possible behavioural scenarios of the model.