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.     

An SEIS epidemic model with transport-related infection

In this paper, an SEIS epidemic model is proposed to study the effect of transport-related infection on the spread and control of infectious disease. New result implies that traveling of the exposed (means exposed but not yet infectious) individuals can bring disease from one region to other regions even if the infectious individuals are inhibited from traveling among regions. It is shown that transportation among regions will change the disease dynamics and break infection out even if infectious diseases will go to extinction in each isolated region without transport-related infection. In addition, our analysis shows that transport-related infection intensifies the disease spread if infectious diseases break out to cause an endemic situation in each region, in the sense of that both the absolute and relative size of patients increase. This suggests that it is very essential to strengthen restrictions of passengers once we know infectious diseases appeared.     

Persistence and permanence in a metapopulation model with space-limited recruitment

In this paper we analyze a metapopulation model with space-limited recruitment. The model describes the population dynamics of sessile adult and planktonic larvae in a common larval pool. We introduce the basic reproduction number of each species which is the expected number of future larvae reproduced by one larva. We consider the conditions for the persistence of the multi-species and multi-habitats model and the permanence of the single-species model. Subsequently, we consider the conditions for the existence of the non-trivial steady state of the single-species model and its global stability, and the permanence of the two species and two habitats model.     

An epidemic model in a patchy environment

An epidemic model is proposed to describe the dynamics of disease spread among patches due to population dispersal. We establish a threshold above which the disease is uniformly persistent and below which disease-free equilibrium is locally attractive, and globally attractive when both susceptible and infective individuals in each patch have the same dispersal rate. Two examples are given to illustrate that the population dispersal plays an important role for the disease spread. The first one shows that the population dispersal can intensify the disease spread if the reproduction number for one patch is large, and can reduce the disease spread if the reproduction numbers for all patches are suitable and the population dispersal rate is strong. The second example indicates that a population dispersal results in the spread of the disease in all patches, even though the disease can not spread in each isolated patch.     

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.     

Impulsive SUI epidemic model for HIV/AIDS with chronological age and infection age

This paper develops an impulsive SUI model of human immunodeficiency virus/acquired immunodeficiency syndrome(HIV/AIDS) epidemic for the first time to study the dynamic behavior of this model. The SUI model is described by impulsive partial differential equations. First, the well-posedness of the model is attained by the method of characteristic lines and iterative method. Secondly, the basic reproduction number R₀(q,T) of the epidemic which depends on the impulsive HIV-finding period T and the HIV-finding proportion q is obtained by mathematical analysis. Our result shows that HIV/AIDS epidemic can be theoretically eradicated if we can have the suitable HIV-finding proportion q and the impulsive HIV-finding period T such that R₀(q,T)<1. We also conjecture that the infection-free periodic solution of the SUI model is unstable when R₀(q,T)>1.     

An epidemic model with infector and exposure dependent severity

A stochastic epidemic model allowing for both mildly and severely infectious individuals is defined, where an individual can become severely infectious directly upon infection or if additionally exposed to infection. It is shown that, assuming a large community, the initial phase of the epidemic may be approximated by a suitable branching process and that the main part of an epidemic that becomes established admits a law of large numbers and a central limit theorem, leading to a normal approximation for the final outcome of such an epidemic. Effects of vaccination prior to an outbreak are studied and the critical vaccination coverage, above which only small outbreaks can occur, is derived. The results are illustrated by simulations that demonstrate that the branching process and normal approximations work well for finite communities, and by numerical examples showing that the final outcome may be close to discontinuous in certain model parameters and that the fraction mildly infected may actually increase as an effect of vaccination.     

The role of density-dependent dispersal in source-sink dynamics

I investigate two aspects of source-sink theory that have hitherto received little attention: density-dependent dispersal and the cost of dispersal to sources. The cost arises because emigration reduces the per capita growth rate of sources, thus predisposing them to extinction. I show that source-sink persistence depends critically on the interplay between these two factors. When the emigration rate increases with abundance at an accelerating rate, dispersal costs to sources is the lowest and risk of source-sink extinction the least. When the emigration rate increases with abundance at a decelerating rate, dispersal costs to sources is the highest and the risk of source-sink extinction the greatest. Density-independent emigration has an intermediate effect. Thus, density-dependent dispersal per se does not increase or decrease source-sink persistence relative to density-independent dispersal. The exact mode of dispersal is crucial. A key point to appreciate is that these effects of dispersal on source-sink extinction arise from the temporal density-dependence that dispersal induces in the per capita growth rates of source and sink populations. Temporal density-dependence due to dispersal is beneficial at low abundances because it rescues sinks from extinction, and detrimental at high abundances because it drives otherwise viable sources to extinction. These results are robust to the nature of population dynamics in the sink, whether exponential or logistic. They provide a means of assessing the relative costs and benefits of preserving sink habitats given three biological parameters.     

一类带有肝炎B病毒感染的数学模型的全局稳定性分析（英文）

本文主要分析了一类具有肝炎B病毒感染且带有治愈率的典型的数学模型（HBV）.通过稳定性分析,得到了该模型的无病平衡点与地方病平衡点全局稳定的充分条件,并且证明了当基本再生数R0〈1, HBV感染消失;当R0〉1,HBV感染持续.     

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’.     

An SIRVS epidemic model with pulse vaccination strategy

The aim of this paper is to analyze an SIRVS epidemic model in which pulse vaccination strategy (PVS) is included. We are interested in finding the basic reproductive number of the model which determine whether or not the disease dies out. The global attractivity of the disease-free periodic solution (DFPS for short) is obtained when the basic reproductive number is less than unity. The disease is permanent when the basic reproductive number is greater than unity, i.e., the epidemic will turn out to endemic. Our results indicate that the disease will go to extinction when the vaccination rate reaches some critical value.     

一类带有肝炎B病毒感染的数学模型的全局稳定性分析

本文主要分析了一类具有肝炎B病毒感染且带有治愈率的典型的数学模型(HBV).通过稳定性分析,得到了该模型的无病平衡点与地方病平衡点全局稳定的充分条件,并且证明了当基本再生数R0＜1,HBV感染消失;当R0＞1,HBV感染持续.     

Age-structured homogeneous epidemic systems with application to the MSEIR epidemic model

In this paper, we develop a new approach to deal with asymptotic behavior of the age-structured homogeneous epidemic systems and discuss its application to the MSEIR epidemic model. For the homogeneous system, there is no attracting nontrivial equilibrium, instead we have to examine existence and stability of persistent solutions. Assuming that the host population dynamics can be described by the stable population model, we rewrite the basic system into the system of ratio age distribution, which is the age profile divided by the stable age profile. If the host population has the stable age profile, the ratio age distribution system is reduced to the normalized system. Then we prove the stability principle that the local stability or instability of steady states of the normalized system implies that of the corresponding persistent solutions of the original homogeneous system. In the latter half of this paper, we prove the threshold and stability results for the normalized system of the age-structured MSEIR epidemic model.      

Dynamical behavior of a hepatitis B virus transmission model with vaccination

Hepatitis B virus (HBV) infection is a globally health problem. In 2005, the WHO Western Pacific Regional Office set a goal of reducing chronic HBV infection rate to less than 2% among children five years of age by 2012, as an interim milestone towards the final goal of less than 1%. Many countries made some plans (such as free HBV vaccination program for all neonates in China now) to control the transmission HBV. We develop a model to explore the impact of vaccination and other controlling measures of HBV infection. The model has simple dynamical behavior which has a globally asymptotically stable disease-free equilibrium when the basic reproduction number R₀≤1, and a globally asymptotically stable endemic equilibrium when R₀>1. Numerical simulation results show that the vaccination is a very effective measure to control the infection and they also give some useful comments on controlling the transmission of HBV.     

On a population pathogen model incorporating species dispersal with temporal variation in dispersal rate

In the present paper, we consider a mathematical model of ecosystem population interaction where the population suffers from a susceptible–infectious–susceptible disease. Dispersal of both the susceptible and the infective is incorporated using reaction–diffusion equations. We first study the stability criteria of the basic (non-spatial) model around the disease-free and the infected steady states. We find that the loss rate of the infective species controls disease prevalence. Also without predation pressure, the disease will continue to exist among the population. Then we analyze the spatial model with species dispersal in constant as well as in time-varying form. It is observed that though constant dispersal is unable to generate diffusion-driven instability, dispersal with sinusoidal variation in dispersion rate can generate diffusive instability when the wave number of the perturbation lies within a given range. Numerical simulations are performed to illustrate analytical studies.     

一类具有阶段结构的病毒动力学模型

在病毒能影响未感染细胞的产生的假设下,本文考虑了一类被感染细胞具有潜伏和活性两阶段的动力学模型,通过对模型进行近似和简化,得到了病毒的基本再生率．当基本再生率小于1时病毒将最终灭绝;当基本再生率大于1时,模型存在唯一的正平衡点,它是局部渐近稳定的,并且病毒持续存在．     

A fully coupled, mechanistic model for infectious disease dynamics in a metapopulation: movement and epidemic duration

The drive to understand the invasion, spread and fade out of infectious disease in structured populations has produced a variety of mathematical models for pathogen dynamics in metapopulations. Very rarely are these models fully coupled, by which we mean that the spread of an infection within a subpopulation affects the transmission between subpopulations and vice versa. It is also rare that these models are accessible to biologists, in the sense that all parameters have a clear biological meaning and the biological assumptions are explained. Here we present an accessible model that is fully coupled without being an individual-based model. We use the model to show that the duration of an epidemic has a highly non-linear relationship with the movement rate between subpopulations, with a peak in epidemic duration appearing at small movement rates and a global maximum at large movement rates. Intuitively, the first peak is due to asynchrony in the dynamics of infection between subpopulations; we confirm this intuition and also show the peak coincides with successful invasion of the infection into most subpopulations. The global maximum at relatively large movement rates occurs because then the infectious agent perceives the metapopulation as if it is a single well-mixed population wherein the effective population size is greater than the critical community size.     

Maximum likelihood estimation of neutral model parameters for multiple samples with different degrees of dispersal limitation

In a recent paper, I presented a sampling formula for species abundances from multiple samples according to the prevailing neutral model of biodiversity, but practical implementation for parameter estimation was only possible when these samples were from local communities that were assumed to be equally dispersal limited. Here I show how the same sampling formula can also be used to estimate model parameters using maximum likelihood when the samples have different degrees of dispersal limitation. Moreover, it performs better than other, approximate, parameter estimation approaches. I also show how to calculate errors in the parameter estimates, which has so far been largely ignored in the development of and debate on neutral theory.     

A two-age-classes dengue transmission model

In this paper, we discuss a two-age-classes dengue transmission model with vaccination. The reason to divide the human population into two age classes is for practical purpose, as vaccination is usually concentrated in one age class. We assume that a constant rate of individuals in the child-class is vaccinated. We analyze a threshold number which is equivalent to the basic reproduction number. If there is an undeliberate vaccination to infectious children, which worsens their condition as the time span of being infectious increases, then paradoxically, vaccination can be counter productive. The paradox, stating that vaccination makes the basic reproduction number even bigger, can occur if the worsening effect is greater than a certain threshold, a function of the human demographic and epidemiological parameters, which is independent of the level of vaccination. However, if the worsening effect is to increase virulence so that one will develop symptoms, then the vaccination is always productive. In both situations, screening should take place before vaccination. In general, the presence of class division has obscured the known rule of thumb for vaccination.     

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.