Invasion threshold in heterogeneous metapopulation networks

We study the dynamics of epidemic and reaction-diffusion processes in metapopulation models with heterogeneous connectivity patterns. In susceptible-infected-removed-like processes, along with the standard local epidemic threshold, the system exhibits a global invasion threshold. We provide an explicit expression of the threshold that sets a critical value of the diffusion/mobility rate below, which the epidemic is not able to spread to a macroscopic fraction of subpopulations. The invasion threshold is found to be affected by the topological fluctuations of the metapopulation network. The results presented provide a general framework for the understanding of the effect of travel restrictions in epidemic containment.     

Disease spreading on fitness-rewired complex networks

As people travel, human contact networks may change topologically from time to time. In this paper, we study the problem of epidemic spreading on this kind of dynamic network, specifically the one in which the rewiring dynamics of edges are carried out to preserve the degree of each node (called fitness rewiring). We also consider the adaptive rewiring of edges, which encourages disconnections from and discourages connections to infected nodes and eventually leads to the isolation of the infected from the susceptible with only a small number of links between them. We find that while the threshold of epidemic spreading remains unchanged and prevalence increases in the fitness rewiring dynamics, meeting of the epidemic threshold is delayed and prevalence is reduced (if adaptive dynamics are included). To understand these different behaviors, we introduce a new measure called the “mean change of effective links” and find that creation and deletion of pathways for pathogen transmission are the dominant factors in fitness and adaptive rewiring dynamics, respectively.     

Epidemic dynamics behavior in some bus transport networks

We abstract bus transport networks (BTNs) to complex networks using the Space P approach. First, we select three actual BTNs in three major cities in China, namely, Beijing, Shanghai and Hangzhou. Using the SIS model, we simulate and study the epidemic spreading in the three BTNs. We obtain the density of infected vertices varying with time and the stationary density of infected vertices varying with infection rate. Second, we simulate and study the epidemic spreading in a recently introduced BTN evolution model, the network properties of which correspond well with those of actual BTNs. Third, we use mean-field theory to analyze the epidemic dynamics behavior of the BTN evolution model and obtain the theoretical epidemic threshold of this model. The theoretical value agrees well with the simulation results. Based on the work in this paper, we provide the following possible forecasts for epidemic dynamics in actual BTNs. An actual BTN should have a finite positive epidemic threshold. If the effective infection rate is above this threshold, the epidemic spread in the network and the density of infected vertices finally stabilizes in a balanced state. Below this threshold, the number of infected vertices decays exponentially fast and the epidemic cannot spread on a large scale.     

Modelling the effect of heterogeneous vaccination on metapopulation epidemic dynamics

Vaccination as an epidemic control strategy has a significant effect on epidemic spreading. In this paper, we propose a novel epidemic spreading model on metapopulation networks to study the impact of heterogeneous vaccination on epidemic dynamics, where nodes represent geographical areas and links connecting nodes correspond to human mobility between areas. Using a mean-field approach, we derive the theoretical spreading threshold revealing a non-trivial dependence on the heterogeneity of vaccination. Extensive Monte Carlo simulations validate the theoretical threshold and also show the complex temporal epidemic behaviours above the threshold.     

在二部无标度网上的两性疾病传播

利用易感-感染-易感(SIS)传播模型研究人类性接触网上的病毒传播.当仅仅考虑异性性接触时,该网络是一个二部的无标度网.对这个网络上的SIS传播模型,通过率方程的方法分析了男性感染率和女性感染率与传染阈值之间的关系,发现女性感染者与男性感染者之比由网络的拓扑和男女感染率之比所确定.这一结果表明性接触网的拓扑对性传染病传播的重要性.最后给出了支持理论结果的数值模拟. 关键词： 性传染病 两性性接触网 无标度网络 二部图     

Epidemic dynamics on an adaptive network

Many real-world networks are characterized by adaptive changes in their topology depending on the state of their nodes. Here we study epidemic dynamics on an adaptive network, where the susceptibles are able to avoid contact with the infected by rewiring their network connections. This gives rise to assortative degree correlation, oscillations, hysteresis, and first order transitions. We propose a low-dimensional model to describe the system and present a full local bifurcation analysis. Our results indicate that the interplay between dynamics and topology can have important consequences for the spreading of infectious diseases and related applications.     

异质自适应网络中的核心-边缘结构及其对疾病传播的抑制作用

节点属性异质自适应网络中疾病传播的研究表明节点属性异质性可以很大程度上增大传播阈值, 并且自组织形成一个更鲁棒的度异质网络结构. 本文从数值模拟方面研究鲁棒的度分布异质结构的自组织形成过程, 分析发现核心-边缘结构的形成才是导致传播阈值增大的根本原因. 鉴于此, 提出一种重连策略, 能够促进核心-边缘结构的形成, 从而达到增大传播阈值的目的. 这不仅有助于深入认识节点属性异质自适应网络中的流行病传播过程, 而且为疾病传播控制策略的提出提供了新思路.     

Synchronizability of chaotic logistic maps in delayed complex networks

We study a network of coupled logistic maps whose interactions occur with a certain distribution of delay times. The local dynamics is chaotic in the absence of coupling and thus the network is a paradigm of a complex system. There are two regimes of synchronization, depending on the distribution of delays: when the delays are sufficiently heterogeneous the network synchronizes on a steady-state (that is unstable for the uncoupled maps); when the delays are homogeneous, it synchronizes in a time-dependent state (that is either periodic or chaotic). Using two global indicators we quantify the synchronizability on the two regimes, focusing on the roles of the network connectivity and the topology. The connectivity is measured in terms of the average number of links per node, and we consider various topologies (scale-free, small-world, star, and nearest-neighbor with and without a central hub). With weak connectivity and weak coupling strength, the network displays an irregular oscillatory dynamics that is largely independent of the topology and of the delay distribution. With heterogeneous delays, we find a threshold connectivity level below which the network does not synchronize, regardless of the network size. This minimum average number of neighbors seems to be independent of the delay distribution. We also analyze the effect of self-feedback loops and find that they have an impact on the synchronizability of small networks with large coupling strengths. The influence of feedback, enhancing or degrading synchronization, depends on the topology and on the distribution of delays.     

一种基于元胞自动机的自适应网络病毒传播模型

自适应网络是节点动力学和网络动力学相互作用和反馈的演化网络. 基于元胞自动机建立自适应网络中易感-感染-易感(susceptible-infected-susceptible)的病毒传播模型,研究节点为了规避病毒传播所采取的多种网络重连规则对病毒传播及网络统计特征的影响. 结果表明:自适应网络中的重连规则可以有效减缓病毒传播速度,降低病毒传播规模;随机重连规则使得网络统计特征趋于随机网络;基于元胞自动机建立的传播模型清晰地表达了病毒在传播过程中的双稳态现象. 关键词： 自适应网络 传播动力学 网络动力学 元胞自动机     

Finite size effects in epidemic spreading: the problem of overpopulated systems

In this paper we analyze the impact of network size on the dynamics of epidemic spreading. In particular, we investigate the pace of infection in overpopulated systems. In order to do that, we design a model for epidemic spreading on a finite complex network with a restriction to at most one contamination per time step, which can serve as a model for sexually transmitted diseases spreading in some student communes. Because of the highly discrete character of the process, the analysis cannot use the continuous approximation widely exploited for most models. Using a discrete approach, we investigate the epidemic threshold and the quasi-stationary distribution. The main results are two theorems about the mixing time for the process: it scales like the logarithm of the network size and it is proportional to the inverse of the distance from the epidemic threshold.     

Contagion dynamics on adaptive multiplex networks with awareness-dependent rewiring

Over the last few years, the interplay between contagion dynamics of social influences (e.g., human awareness, risk perception, and information dissemination) and biological infections has been extensively investigated within the framework of multiplex networks. The vast majority of existing multiplex network spreading models typically resort to heterogeneous mean-field approximation and microscopic Markov chain approaches. Such approaches usually manifest richer dynamical properties on multiplex networks than those on simplex networks; however, they fall short of a subtle analysis of the variations in connections between nodes of the network and fail to account for the adaptive behavioral changes among individuals in response to epidemic outbreaks. To transcend these limitations, in this paper we develop a highly integrated effective degree approach to modeling epidemic and awareness spreading processes on multiplex networks coupled with awareness-dependent adaptive rewiring. This approach keeps track of the number of nearest neighbors in each state of an individual; consequently, it allows for the integration of changes in local contacts into the multiplex network model. We derive a formula for the threshold condition of contagion outbreak. Also, we provide a lower bound for the threshold parameter to indicate the effect of adaptive rewiring. The threshold analysis is confirmed by extensive simulations. Our results show that awareness-dependent link rewiring plays an important role in enhancing the transmission threshold as well as lowering the epidemic prevalence. Moreover, it is revealed that intensified awareness diffusion in conjunction with enhanced link rewiring makes a greater contribution to disease prevention and control. In addition, the critical phenomenon is observed in the dependence of the epidemic threshold on the awareness diffusion rate, supporting the metacritical point previously reported in literature. This work may shed light on understanding of the interplay between epidemic dynamics and social contagion on adaptive networks.     

Disease spreading in structured scale-free networks

We study the spreading of a disease on top of structured scale-free networks recently introduced. By means of numerical simulations we analyze the SIS and the SIR models. Our results show that when the connectivity fluctuations of the network are unbounded whether the epidemic threshold exists strongly depends on the initial density of infected individuals and the type of epidemiological model considered. Analytical arguments are provided in order to account for the observed behavior. We conclude that the peculiar topological features of this network and the absence of small-world properties determine the dynamics of epidemic spreading. Received 16 October 2002 Published online 4 February 2003 RID="a" ID="a"e-mail: yamir@ictp.trieste.it     

多关系网络上的流行病传播动力学研究

多关系网络已经吸引了许多人的注意, 目前的研究主要涉及其拓扑结构及其演化的分析、 不同类型关系的挖掘、重叠社区的检测、级联失效动力学等. 然而,多关系网络上流行病传播的研究还相对较少. 由此提出一种双关系网络模型(工作-朋友关系网), 研究多关系对于流行病传播动力学行为的影响. 在全接触模式下, 多关系的存在会显著降低网络中的爆发阈值, 使得疾病更容易流行而难以控制. 对比ER (Erdös-Rènyi), WS (Watts-Strogatz), BA (Barabási-Albert)三种网络, 由于结构异质性的差异, WS网络受到的影响最大, ER网络次之, BA网络最小. 有趣的是, 其爆发阈值的相对变化大小与网络结构无关. 在单点接触模式下, 增加强关系的权重将显著提升爆发阈值, 降低感染密度; 随着强关系的比例变化将出现最优值现象: 极大的爆发阈值和极小的感染密度. 随着强关系的边权增加, 达到最优值的边比例将减少. 更为有趣的是, 三个网络中优值出现的位置几乎一致, 独立于网络结构. 这一研究不但有助于理解多关系网络上的病毒传播过程, 也为多关系网络研究提供了一个新的视角. 关键词： 多关系网络 流行病传播 接触模式 爆发阈值     

Thresholds for epidemic spreading in networks

We study the threshold of epidemic models in quenched networks with degree distribution given by a power-law. For the susceptible-infected-susceptible model the activity threshold λ(c) vanishes in the large size limit on any network whose maximum degree k(max) diverges with the system size, at odds with heterogeneous mean-field (HMF) theory. The vanishing of the threshold has nothing to do with the scale-free nature of the network but stems instead from the largest hub in the system being active for any spreading rate λ>1/√k(max) and playing the role of a self-sustained source that spreads the infection to the rest of the system. The susceptible-infected-removed model displays instead agreement with HMF theory and a finite threshold for scale-rich networks. We conjecture that on quenched scale-rich networks the threshold of generic epidemic models is vanishing or finite depending on the presence or absence of a steady state.     

Modular Epidemic Spreading in Small-World Networks

We study the epidemic spreading of the susceptible-infected-susceptible model on small-world networks with modular structure. It is found that the epidemic threshold increases linearly with the modular strength. Furthermore, the modular structure may influence the infected density in the steady state and the spreading velocity at the beginning of propagation. Practically, the propagation can be hindered by strengthening the modular structure in the view of network topology. In addition, to reduce the probability of reconnection between modules may also help to control the propagation.     

基于交通流量的病毒扩散动力学研究

不同于经典扩散模型中节点传染力等同于节点度k的假定, 基于交通流量的病毒扩散模型中, 各个节点的传染力可以等同于节点实际介数b_k. 利用平均场近似方法, 提出基于交通流量SIS病毒修正扩散模型. 根据修正SIS模型, 以最小搜索信息路由为例, 重新研究病毒传播率β, 平均发包率λ同传播阈值β_c, 平稳状态病毒密度ρ之间的关系. 理论分析与实验结果均表明, 当网络拓扑和路由策略一定时, 传播阈值β_c为实际介数b_k的均值<b_k>与其平方的均值<b_k²>的比值. 而稳定状态时感染密度ρ同感染同病毒传播率β, 平均发包率λ 以及λ =1时节点实际介数的均值<b_λ=1> 的乘积倒数存在幂率关系.     

Epidemic threshold and phase transition in scale-free networks with asymmetric infection

We study the SIS epidemic dynamics on scale-freeweighted networks with asymmetric infection, by both analysis andnumerical simulations, with focus on the epidemic threshold aswell as critical behaviors. It is demonstrated that the asymmetryof infection plays an important role: we could redistribute theasymmetry to balance the degree heterogeneity of the network andthen to restore the epidemic threshold to a fnite value. On theother hand, we show that the absence of the epidemic threshold isnot so bad as commented previously since the prevalence grows veryslowly in this case and one could only protect a few vertices toprevent the diseases propagation.     

Dynamical behaviour of an epidemic on complex networks with population mobility

In this paper, we study the dynamical behaviour of an epidemic on complex networks with population mobility. In our model, the number of people on each node is unrestricted as the nodes of the network are considered as cities, communities, and so on. Because people can travel between different cities, we study the effect of a population's mobility on the epidemic spreading. In view of the population's mobility, we suppose that the susceptible individual can be infected by an infected individual in the same city or other connected cities. Simulations are presented to verify our analysis.     

Epidemic prevalence on random mobile dynamical networks: individual heterogeneity and correlation

In this paper, we extend the susceptible-infected-susceptible (SIS) epidemiological model on a random dynamical network composed of mobile individuals, in which the infection is caused by the collisions between susceptible and infected individuals at the spreading rate proportional to their susceptibilities and infectivities. We analytically study the criticality of spreading dynamics under different distributions of individual susceptibility and infectivity, and numerically verify the cases of power-law and (or) Gaussian distributions. Our findings show that the heterogeneity of individual susceptibility and infectivity increases the epidemic threshold, and the positive correlation of individual susceptibility and infectivity avails to the epidemic prevalence.     

Multiple routes transmitted epidemics on multiplex networks

This letter investigates the multiple routes transmitted epidemic process on multiplex networks. We propose detailed theoretical analysis that allows us to accurately calculate the epidemic threshold and outbreak size. It is found that the epidemic can spread across the multiplex network even if all the network layers are well below their respective epidemic thresholds. Strong positive degree–degree correlation of nodes in multiplex network could lead to a much lower epidemic threshold and a relatively smaller outbreak size. However, the average similarity of neighbors from different layers of nodes has no obvious effect on the epidemic threshold and outbreak size.