含有免疫策略的一类计算机病毒模型稳定性分析

建立计算机病毒的动力学数学模型,可以更好地揭示计算机病毒流行的原因.考虑到免疫策略对计算机病毒动力学模型的重要影响,对一类SEIR模型进行了改进.得到了模型的无感染平衡点和感染平衡点的存在性,并分别求得两类平衡点的渐近稳定条件,通过数值模拟展示了理论成果.     

传播动力学模型回顾与展望

传播动力学模型主要包括传染病动力学模型、计算机病毒传播模型以及谣言传播模型.首先从传染病动力学模型入手,分别介绍均匀混合传染病动力学模型和网络动力学模型;然后介绍计算机病毒传播模型以及谣言传播模型,并与传染病模型进行对比.最后作了总结与展望.     

广义网络上的计算机病毒传播模型

为了研究计算机病毒在广义网络中传播的机制,文章分别提出了计算机病毒传播的非线性和线性模型.理论分析表明,网络的最大特征值是决定计算机病毒传播的重要参数.其次,文章给出非线性和线性模型中的无病毒均衡点全局稳定的充分条件,同时也证明了线性模型的有病毒平衡点的全局吸引性.最后,通过一些数学模拟实验验证了理论分析的主要结论.     

BA无标度网络中的SIR模型

网络化是现代世界的一个重要特征,不仅包括互联网,还包括航空网,人际关系网,而它们都是很典型的无标度网络.在BA无标度网中,结合经典的SIR模型,建立了新的SIR模型,并对模型进行了研究,得到了BA无标度网络对传染病与计算机病毒传播具有脆弱性的结论.     

一类时滞分数阶计算机病毒模型的稳定性研究

本文研究一类改进的时滞分数阶计算机病毒模型正平衡点的稳定性问题.利用线性化方法和拉普拉斯变换获得模型对应的线性化系统的特征方程,通过讨论特征方程的根以及横截条件研究时滞和正平衡点稳定性之间的关系,推导了Hopf分支出现时时滞临界值的计算公式,并选择恰当的系统参数进行数值模拟以验证理论分析的合理性.     

具有非线性传染率和时滞的随机SIQR计算机病毒模型的渐近行为

研究了一类具有非线性发生率和时滞的随机SIQR计算机病毒模型.首先证明了该系统具有唯一的全局正解,然后通过构造适当的Lyapunov函数并利用伊藤公式,分析了该模型的解在无病平衡点附近及地方病平衡点附近的渐近行为,最后通过数值模拟对随机系统解的渐近行为做了进一步的分析并给出了结论.     

图的存活率与消防员问题

消防员问题可视为传染病、火灾、谣言、计算机病毒等传播的一个简化模型.假设一把火在一个图的某个点或多个点燃起,消防员选择若干个未着火的顶点进行防护,然后火蔓延到前一步着火点的未燃邻点.当火不再蔓延时整个过程结束.消防员问题自1995年提出以来引起了人们的广泛关注.本文简述了与消防员问题相关的最近研究进展,包括算法复杂性、无限图和有向图的消防员问题、图的存活率、图的燃烧数及一些有待于进一步研究的问题.     

心理素质诊断模型的建立与应用

综合运用国内外多种测量量表对大学生的心理素质进行诊断与测试 ,并应用多元统计分析方法对其心理素质结构主因素进行定量分析 ,在此基础上建立了心理素质诊断模型 ,并运用该模型对实际问题进行了分析 .     

区间多属性决策问题研究综述

从区间数决策矩阵的规范化方法、属性权重的确定及区间数决策矩阵的排序方法三方面对现有的区间多属性决策问题研究的主要成果进行了归纳和总结,并对研究方法进行了分析和评价,最后对全文进行了总结,并探讨了该问题未来的研究前景.     

基于DEA结果修正模型的公路网交通效益评价

为了更好地对公路网建设的交通效益进行评价,构建了公路网交通效益指标体系,并采用数据包络分析(DEA)方法进行相对有效性评价与分析.鉴于全排序的客观要求,在CCR的基础上提出了基于系统潜能损失的结果修正模型,并引入了最劣决策单元对其进行DEA再评价.以9个公路网为蓝本采集指标数据,进行了基于DEA结果修正模型的交通效益评价,并与选取的9个公路网的实际运行情况做了对比分析.     

一类病毒自身发生变异的传染病模型的近似解

针对一类病毒变异前后传染病患者具有不同传染率的情形,利用同伦映射方法,得到其相应分阶段传播的动力学生态模型的渐近解.     

Dynamical behaviors of a discrete HIV‐1 virus model with bilinear infective rate

We establish a discrete virus dynamic model by discretizing a continuous HIV‐1 virus model with bilinear infective rate using ‘hybrid’ Euler method. We discuss not only the existence and global stability of the uninfected equilibrium but also the existence and local stability of the infected equilibrium. We prove that there exists a crucial value similar to that of the continuous HIV‐1 virus dynamics, which is called the basic reproductive ratio of the virus. If the basic reproductive ratio of the virus is less than one, the uninfected equilibrium is globally asymptotically stable. If the basic reproductive ratio of the virus is larger than one, the infected equilibrium exists and is locally stable. Moreover, we consider the permanence for such a system by constructing a Lyapunov function v_n. Copyright © 2013 John Wiley & Sons, Ltd.     

A compartmental model to explore the interplay between virus epidemics and honeynet potency

Honeynet technology is an active approach that is used to capture novel viruses and provide feedback on a matching immunization strategy. A compartmental model is formulated and analyzed to explore the interplay between virus epidemics and potency of a heterogeneous honeynet. Theoretical analysis of the model shows the conditions under which the minimum amount and best location in configuring a honeynet are determined. Furthermore, the honeypot with more system vulnerabilities is beneficial for mitigating the virus epidemic to a lower level, whereas the honeynet with a lower power law index is better for acquiring the virus samples. A number of numerical examples are presented to illustrate the theoretical analysis. On the basis of the results, some ideas for imposing restrictions on the spread of virus or improving the design of a honeynet are suggested.     

Generals die in friendly fire,or modeling immune response to HIV

We develop a kinetic model for CD8 T lymphocytes (CTL) whose purpose is to kill cells infected with viruses and intracellular parasites. Using a set of first-order nonlinear differential equations, the model predicts how numbers of different cell types involved in CTL response depend on time. The model postulates that CTL response requires continuous presence of professional antigen-presenting cells (APC) comprised of macrophages and dendritic cells. It assumes that any virus present in excess of a threshold level activates APC that, in turn, activate CTL that expand in number and become armed “effector” cells. In the end, APC are deactivated after virus is cleared. The lack of signal from APC causes effector cells to differentiate, by default, into “transitory cells” that either die, or, in a small part, become long-lived memory cells. Viruses capable of infecting APC will cause premature retirement of effector CTL. If transitory cells encounter virus, which takes place after the premature depletion, CTL become anergic (unresponsive to external stimuli). The model is designed to fit recent experiments on primary CTL response to simian immunodeficiency virus closely related to HIV and lymphocytic choriomeningitis virus. The two viruses are known to infect APC and make them targets for CTL they are supposed to control. Both viruses cause premature depletion and anergy of CTL and persist in the host for life.     

A bi-virus competing model with time-varying susceptibility and repeated infection

This paper introduces a bi-virus model with time-varying susceptibility. The model describes the case that there coexist two viruses and the time-varying susceptibility due to repeated infections. For different parameters, we investigate the stability of various equilibriums. Under appropriate conditions the two viruses show competitive relationship, that is, one virus will eventually become a pandemic, and the other virus will eventually disappear. For this case, we further study the dynamical behavior of virus transmission. The model shows some new phenomena, that is, the outbreak of the virus will be delayed appropriately, giving people an illusion. Finally, we present a numerical example to illustrate the effectiveness of the theoretical results.     

The impact of patch forwarding on the prevalence of computer virus: A theoretical assessment approach

Virus patches can be disseminated rapidly through computer networks and take effect as soon as they have been installed, which significantly enhances their virus-containing capability. This paper aims to theoretically assess the impact of patch forwarding on the prevalence of computer virus. For that purpose, a new malware epidemic model, which takes into full account the influence of patch forwarding, is proposed. The dynamics of the model is revealed. Specifically, besides the permanent susceptible equilibrium, this model may admit an infected or a patched or a mixed equilibrium. Criteria for the global stability of the four equilibria are given, respectively, accompanied with numerical examples. The obtained results show that the spectral radii of the patch-forwarding network and the virus-spreading network both have a marked impact on the prevalence of computer virus. The influence of some key factors on the prevalence of virus is also revealed. Based on these findings, some strategies of containing electronic virus are recommended.     

Global properties of an improved hepatitis B virus model

Hepatitis B virus (HBV) infection is an important health problem worldwide. In this paper, we introduce an improved HBV model with standard incidence function and cytokine-mediated ‘cure’ based on empirical evidences. By carrying out a global analysis of the modified model and studying the stability of the equilibria, we show that infection-free equilibrium is globally asymptotically stable if the basic reproduction number of virus is less than one and, conversely, the infection equilibrium is globally asymptotically stable if the basic reproduction number of virus is greater than one. The study and information derived from this model and other related models may have an important impact on preventing mortality due to hepatitis B virus in the future.     

Existence of positive periodic solution of a hepatitis B virus infection model

In this paper, a periodic model for hepatitis B virus infection is proposed. The model describes the breeding of the infected cells and the periodic variation of the environment. On the basis of the continuation theorem of coincidence degree theory, a condition for the existence of a positive periodic solution to the model is established. The result can be used to explain the wave phenomenon on the density of the pathogens in patients blood and the occurrence of superinfection in hepatitis B virus infections. Copyright © 2014 John Wiley & Sons, Ltd.     

Mathematical analysis of a virus dynamics model with general incidence rate and cure rate

The rate of infection in many virus dynamics models is assumed to be bilinear in the virus and uninfected target cells. In this paper, the dynamical behavior of a virus dynamics model with general incidence rate and cure rate is studied. Global dynamics of the model is established. We prove that the virus is cleared and the disease dies out if the basic reproduction number R₀≤1 while the virus persists in the host and the infection becomes endemic if R₀>1.     

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.