一类具有潜伏期的传染病模型的稳定性研究

研究了一类潜伏期和感染期均有传染力的SEIQR模型,借助于轨道稳定性,Jacobian矩阵等方法,得到了疾病消亡的阈值——基本再生数R_0,通过构造Lyapunov函数,证明了无病平衡点及地方病平衡点的存在性及全局稳定性.     

具垂直传染和连续预防接种的SIRS传染病模型的研究

研究了具有垂直传染的两类连续预防接种传染病模型,分别给出了SIRS传染病模型基本再生数并利用广义Dulac函数方法和LaSalle不变原理证明了无病平衡点和正平衡点的全局稳定性.最后对两种结果进行了比较.     

具有时变接触率与接种率的脉冲传染病模型研究

讨论了时变接触率和时变接种率的传染病模型,模型中考虑对易感者和染病者同时接种.通过计算得到了判别疾病流行与否的阈值.证明了当基本再生数小于1时,疾病是流行的;当基本再生数大于1时,疾病将成为地方病.     

具有潜伏和隔离的传染病模型的全局稳定性

研究了一类具有隔离仓室和潜伏仓室的非线性高维自治微分系统SEQIJR传染病模型,得到疾病绝灭与否的阀值一基本再生数R0．证明了当R0≤1时,模型仅存在无病平衡点,且无病平衡点是全局渐近稳定的,疾病最终绝灭;当R0〉1时,模型存在两个平衡点,无病平衡点不稳定,地方病平衡点全局渐近稳定,疾病将持续．隔离措施影响着基本再生数,进而推得结论：适当地增大隔离强度,将有益于有效地控制疾病的蔓延．这就从理论上揭示了隔离对疾病控制的积极作用．     

一类与环境因素有关的具有预防接种和双线性疾病发生率的传染病动力学模型研究

本文研究一类与环境有关的SVIBR的传染病模型,得到了基本再生数0R证明了当0R1时无病平衡点全局渐近稳定。     

一类具有常数迁入且总入口在变化的SIRI传染病模型的稳定性

讨论一类具有常数迁入率,染病类有病死且有效接触率依赖于总人数的SIRI传染病模型.给出了基本再生数σ的表达式.如果σ≤1,则疾病消除平衡点是全局稳定的;如果σ＞1,则存在唯一的传染病平衡点且是局部渐近稳定的.对具有双线性传染率和标准传染率的相应模型,进一步证明了当σ＞1时传染病平衡点的全局稳定性.     

具有脉冲出生和脉冲接种的SIR传染病模型

考虑了脉冲出生、脉冲接种、垂直传染、因病死亡等因素,建立了脉冲出生和脉冲接种同时进行的SIR传染病模型,通过分析无病周期解的存在性以及稳定性,得出疾病灭绝的条件.     

一类带有接种和年龄结构的SVIR传染病模型

数学地分析了一类带有接种和年龄结构的SVIR传染病模型的动力学性质,得到了接种疫苗策略φ和年龄a有关的基本再生数R(φ,a)的表达式,证明了当R(0,a)1时,系统中无病平衡态是全局渐近稳定的;当R(φ,a)1时,无病平衡态是不稳定的,此时系统至少存在一地方病平衡态.     

北京市手足口病的流行趋势预测

根据手足口病具有潜伏期的特征,提出了手足口病的SEIR模型框图,并据此建立微分方程模型.通过北京市近年来手足口病疫情周报数据,对参数进行估计并计算基本再生数,预测北京市2014年手足口病的流行趋势,对北京市手足口病的预防控制提供参考.     

带有潜伏期的疾病在捕食系统中的传播（英文）

利用了传染病的SEI模型和捕食-被捕食模型研究了疾病的传染过程.疾病可以在被捕食者之间传染并且也可以在又被捕食者传染给捕食者,但是不会在捕食者之间传染.进一步,我们考虑了疾病在被捕食者之间具有潜伏期.利用布鲁氏菌病作为主要对象,文章建立了非线性微分方程组,并利用定性理论与基本再生数的相关结论证明了所有非负平衡点的稳定条件,并通过数值解讨论了一些生物现象.最后讨论了疾病的传染率和捕食率对系统稳定性的影响以及其他参数对系统可能存在的影响.     

Modeling relapse in infectious diseases

An integro-differential equation is proposed to model a general relapse phenomenon in infectious diseases including herpes. The basic reproduction number R(0) for the model is identified and the threshold property of R(0) established. For the case of a constant relapse period (giving a delay differential equation), this is achieved by conducting a linear stability analysis of the model, and employing the Lyapunov-Razumikhin technique and monotone dynamical systems theory for global results. Numerical simulations, with parameters relevant for herpes, are presented to complement the theoretical results, and no evidence of sustained oscillatory solutions is found.     

An SIS patch model with variable transmission coefficients

In this paper, an SIS patch model with non-constant transmission coefficients is formulated to investigate the effect of media coverage and human movement on the spread of infectious diseases among patches. The basic reproduction number R₀ is determined. It is shown that the disease-free equilibrium is globally asymptotically stable if R₀?1, and the disease is uniformly persistent and there exists at least one endemic equilibrium if R₀>1. In particular, when the disease is non-fatal and the travel rates of susceptible and infectious individuals in each patch are the same, the endemic equilibrium is unique and is globally asymptotically stable as R₀>1. Numerical calculations are performed to illustrate some results for the case with two patches.     

Model-consistent estimation of the basic reproduction number from the incidence of an emerging infection

We investigate the merit of deriving an estimate of the basic reproduction number early in an outbreak of an (emerging) infection from estimates of the incidence and generation interval only. We compare such estimates of with estimates incorporating additional model assumptions, and determine the circumstances under which the different estimates are consistent. We show that one has to be careful when using observed exponential growth rates to derive an estimate of , and we quantify the discrepancies that arise.      

The role of screening and treatment in the transmission dynamics of HIV/AIDS and tuberculosis co-infection: a mathematical study

In this paper, we present a deterministic non-linear mathematical model for the transmission dynamics of HIV and TB co-infection and analyze it in the presence of screening and treatment. The equilibria of the model are computed and stability of these equilibria is discussed. The basic reproduction numbers corresponding to both HIV and TB are found and we show that the disease-free equilibrium is stable only when the basic reproduction numbers for both the diseases are less than one. When both the reproduction numbers are greater than one, the co-infection equilibrium point may exist. The co-infection equilibrium is found to be locally stable whenever it exists. The TB-only and HIV-only equilibria are locally asymptotically stable under some restriction on parameters. We present numerical simulation results to support the analytical findings. We observe that screening with proper counseling of HIV infectives results in a significant reduction of the number of individuals progressing to HIV. Additionally, the screening of TB reduces the infection prevalence of TB disease. The results reported in this paper clearly indicate that proper screening and counseling can check the spread of HIV and TB diseases and effective control strategies can be formulated around ‘screening with proper counseling’.     

Approximation of the Basic Reproduction Number <Emphasis Type="Italic">R</Emphasis><Subscript>0</Subscript> for Vector-Borne Diseases with a Periodic Vector Population

The main purpose of this paper is to give an approximate formula involving two terms for the basic reproduction number R ₀ of a vector-borne disease when the vector population has small seasonal fluctuations of the form p(t) = p ₀ (1+ε cos (ωt − φ)) with ε ≪ 1. The first term is similar to the case of a constant vector population p but with p replaced by the average vector population p ₀. The maximum correction due to the second term is (ε²/8)% and always tends to decrease R ₀. The basic reproduction number R ₀ is defined through the spectral radius of a linear integral operator. Four numerical methods for the computation of R ₀ are compared using as example a model for the 2005/2006 chikungunya epidemic in La Réunion. The approximate formula and the numerical methods can be used for many other epidemic models with seasonality. MSC 92D30 ⋅ 45C05 ⋅ 47A55     

A qualitative analysis of a model for the transmission of varicella-zoster virus

Varicella-zoster virus (VZV) is a herpesvirus which is the known agent for causing varicella (chickenpox) in its initial manifestation and zoster (shingles) in a reactivated state. The standard SEIR compartmental model is modified to include the cycle of shingles acquisition, recovery, and possible reacquisition. The basic reproduction number R(0) shows the influence of the zoster cycle and how shingles can be important in maintaining VZV in populations. The model has the typical threshold behavior in the sense that when R(0)1, the virus persists over time and so chickenpox and shingles remain endemic.     

A habitat-based model for the spread of hantavirus between reservoir and spillover species

New habitat-based models for spread of hantavirus are developed which account for interspecies interaction. Existing habitat-based models do not consider interspecies pathogen transmission, a primary route for emergence of new infectious diseases and reservoirs in wildlife and man. The modeling of interspecies transmission has the potential to provide more accurate predictions of disease persistence and emergence dynamics. The new models are motivated by our recent work on hantavirus in rodent communities in Paraguay. Our Paraguayan data illustrate the spatial and temporal overlaps among rodent species, one of which is the reservoir species for Jabora virus and others which are spillover species. Disease transmission occurs when their habitats overlap. Two mathematical models, a system of ordinary differential equations (ODE) and a continuous-time Markov chain (CTMC) model, are developed for spread of hantavirus between a reservoir and a spillover species. Analysis of a special case of the ODE model provides an explicit expression for the basic reproduction number, , such that if , then the pathogen does not persist in either population but if , pathogen outbreaks or persistence may occur. Numerical simulations of the CTMC model display sporadic disease incidence, a new behavior of our habitat-based model, not present in other models, but which is a prominent feature of the seroprevalence data from Paraguay. Environmental changes that result in greater habitat overlap result in more encounters among various species that may lead to pathogen outbreaks and pathogen establishment in a new host.     

Bifurcation analysis of the Nowak-Bangham model in CTL dynamics

This paper investigates the local bifurcations of a CTL response model published by Nowak and Bangham [M.A. Nowak, C.R.M. Bangham, Population dynamics of immune responses to persistent viruses, Science 272 (1996) 74]. The Nowak-Bangham model can have three equilibria depending on the basic reproduction number, and generates a Hopf bifurcation through two bifurcations of equilibria. The main result shows a sufficient condition for the interior equilibrium to have a unique bifurcation point at which a simple Hopf bifurcation occurs. For this proof, some new techniques are developed in order to apply the method established by Liu [W.M. Liu, Criterion of Hopf bifurcations without using eigenvalues, J. Math. Anal. Appl. 182 (1) (1994) 250]. In addition, to demonstrate the result obtained theoretically, some bifurcation diagrams are presented with numerical examples.     

The control of vector-borne disease epidemics

The theoretical underpinning of our struggle with vector-borne disease, and still our strongest tool, remains the basic reproduction number, R₀, the measure of long term endemicity. Despite its widespread application, R₀ does not address the dynamics of epidemics in a model that has an endemic equilibrium. We use the concept of reactivity to derive a threshold index for epidemicity, E₀, which gives the maximum number of new infections produced by an infective individual at a disease free equilibrium. This index describes the transitory behavior of disease following a temporary perturbation in prevalence. We demonstrate that if the threshold for epidemicity is surpassed, then an epidemic peak can occur, that is, prevalence can increase further, even when the disease is not endemic and so dies out. The relative influence of parameters on E₀ and R₀ may differ and lead to different strategies for control. We apply this new threshold index for epidemicity to models of vector-borne disease because these models have a long history of mathematical analysis and application. We find that both the transmission efficiency from hosts to vectors and the vector-host ratio may have a stronger effect on epidemicity than endemicity. The duration of the extrinsic incubation period required by the pathogen to transform an infected vector to an infectious vector, however, may have a stronger effect on endemicity than epidemicity. We use the index E₀ to examine how vector behavior affects epidemicity. We find that parasite modified behavior, feeding bias by vectors for infected hosts, and heterogeneous host attractiveness contribute significantly to transitory epidemics. We anticipate that the epidemicity index will lead to a reevaluation of control strategies for vector-borne disease and be applicable to other disease transmission models.