Variability of contact process in complex networks

We study numerically how the structures of distinct networks influence the epidemic dynamics in contact process. We first find that the variability difference between homogeneous and heterogeneous networks is very narrow, although the heterogeneous structures can induce the lighter prevalence. Contrary to non-community networks, strong community structures can cause the secondary outbreak of prevalence and two peaks of variability appeared. Especially in the local community, the extraordinarily large variability in early stage of the outbreak makes the prediction of epidemic spreading hard. Importantly, the bridgeness plays a significant role in the predictability, meaning the further distance of the initial seed to the bridgeness, the less accurate the predictability is. Also, we investigate the effect of different disease reaction mechanisms on variability, and find that the different reaction mechanisms will result in the distinct variabilities at the end of epidemic spreading.     

Epidemic spreading in lattice-embedded scale-free networks

We study geographical effects on the spread of diseases in lattice-embedded scale-free networks. The geographical structure is represented by the connecting probability of two nodes that is related to the Euclidean distance between them in the lattice. By studying the standard susceptible-infected model, we found that the geographical structure has great influences on the temporal behavior of epidemic outbreaks and the propagation in the underlying network: the more geographically constrained the network is, the more smoothly the epidemic spreads, which is different from the clearly hierarchical dynamics that the infection pervades the networks in a progressive cascade across smaller-degree classes in Barabási–Albert scale-free networks.     

同时考虑传染媒介和传播延迟的复杂网络病毒传播行为研究

提出一种新的流行病传播模型,基于平均场理论,研究传染媒介和传播延迟同时存在对网络中流行病传播行为的影响.理论分析和仿真结果表明,传染媒介和传播延迟同时存在显著增强了网络中流行病爆发的危险性,并加速了流行病的传播.研究还发现,对于给定的有效传播率,均匀网络中流行病的感染程度分别与传染媒介的传染概率和传播延迟呈对数关系,无标度网络中流行病的感染程度与传染媒介的传染概率呈幂率关系,而与传播延迟之间则存在线性关系。     

复杂网络中考虑不完全免疫的病毒传播研究

复杂网络中不完全免疫包括免疫失败和免疫失效两种情况,本文研究两者同时存在对网络病毒传播行为的影响,基于平均场理论,提出一种新的传播模型.理论分析表明,免疫失败和免疫失效同时存在显著降低了网络的传播临界值,增强了病毒的感染程度.根据传播临界值与免疫节点密度、免疫成功率以及免疫失效率之间的关系,给出有效控制网络病毒传播的策略.通过数值仿真进行验证。     

Statistical model for the effects of phase and momentum randomization on electron transport

In this paper, the study of epidemic spreading of mobile individuals on networks focuses on the system in which each node of the network may be occupied by either one individual or a void, and each individual could move to a neighbour void node. It is found that for the susceptible-infected-susceptible (SIS) model, the diffusion increases the epidemic threshold for arbitrary heterogeneous networks having the degree fluctuations, and the diffusion doesn??t affect the epidemic threshold for regular random networks. In the SI model, the diffusion suppresses the epidemic spread at the early outbreak stage, which indicates that the growth time scale of outbreaks is monotonically increasing with diffusion rate d. The heterogeneous mean-field analysis is in good agreement with the numerical simulations on annealed networks.     

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     

Velocity and hierarchical spread of epidemic outbreaks in scale-free networks

We study the effect of the connectivity pattern of complex networks on the propagation dynamics of epidemics. The growth time scale of outbreaks is inversely proportional to the network degree fluctuations, signaling that epidemics spread almost instantaneously in networks with scale-free degree distributions. This feature is associated with an epidemic propagation that follows a precise hierarchical dynamics. Once the highly connected hubs are reached, the infection pervades the network in a progressive cascade across smaller degree classes. The present results are relevant for the development of adaptive containment strategies.     

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.     

Temporal behaviors of epidemic spreading on the scale-free network

Exploring temporal behaviors of the epidemic spreading is of particular importance, in which field an interesting phenomenon of hierarchical spreading cascade has already been demonstrated. By taking into account the effect of density of infected neighbors around an individual in the definition of spreading rate, an infection mechanism modulated by a parameter is introduced in the present paper. Under the mechanism temporal behaviors on the scale-free network are shown to be different, corresponding to different parameters. Three distinct hierarchical spreading modes are typically exhibited. In addition, a novel way to depict the dynamical processes of the epidemic spreading is also developed and some new features are, thus, clearly displayed.     

Epidemic spreading in scale-free networks including the effect of individual vigilance

In this paper, we study the epidemic spreading in scale-free networks and propose a new susceptible-infected- recovered (SIR) model that includes the effect of individual vigilance. In our model, the effective spreading rate is dynamically adjusted with the time evolution at the vigilance period. Using the mean-field theory, an analytical result is derived. It shows that individual vigilance has no effect on the epidemic threshold. The numerical simulations agree well with the analytical result. Furthermore, we investigate the effect of individual vigilance on the epidemic spreading speed. It is shown that individual vigilance can slow the epidemic spreading speed effectively and delay the arrival of peak epidemic infection.     

基于元胞自动机考虑传播延迟的复杂网络病毒传播研究

基于元胞自动机,研究传播延迟对复杂网络病毒传播动力学行为的影响,提出一种新的易染状态-感染状态-易染状态(SIS)传播模型.研究表明,传播延迟的存在显著降低了网络的传播临界值,增强了网络中病毒爆发的危险性.研究还发现,随着传播延迟的增大,病毒的感染程度以及传播速率都明显增大.此外,SIS传播模型不仅能够反映病毒的平均传播趋势,而且可以描述病毒随时间的动态演化过程以及病毒的爆发和消亡等概率事件,从而有效地克服了利用平均场方法构建的微分方程模型只能反映病毒平均传播趋势的局限性.同时,还给出有效控制网络中病毒传 关键词： 复杂网络 病毒传播 元胞自动机 传播延迟     

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.     

A dynamic epidemic control model on uncorrelated complex networks

In this paper, a dynamic epidemic control model on the uncorrelated complex networks is proposed. By means of theoretical analysis, we found that the new model has a similar epidemic threshold as that of the susceptible-infectedrecovered （SIR） model on the above networks, but it can reduce the prevalence of the infected individuals remarkably. This result may help us understand epidemic spreading phenomena on real networks and design appropriate strategies to control infections.     

Threshold model of cascades in empirical temporal networks

Threshold models try to explain the consequences of social influence like the spread of fads and opinions. Along with models of epidemics, they constitute a major theoretical framework of social spreading processes. In threshold models on static networks, an individual changes her state if a certain fraction of her neighbors has done the same. When there are strong correlations in the temporal aspects of contact patterns, it is useful to represent the system as a temporal network. In such a system, not only contacts but also the time of the contacts are represented explicitly. In many cases, bursty temporal patterns slow down disease spreading. However, as we will see, this is not a universal truth for threshold models. In this work we propose an extension of Watts’s classic threshold model to temporal networks. We do this by assuming that an agent is influenced by contacts which lie a certain time into the past. I.e., the individuals are affected by contacts within a time window. In addition to thresholds in the fraction of contacts, we also investigate the number of contacts within the time window as a basis for influence. To elucidate the model’s behavior, we run the model on real and randomized empirical contact datasets.     

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.     

Communication on the structure of biological networks

Networks are widely used to represent interaction pattern among the components in complex systems. Structures of real networks from different domains may vary quite significantly. As there is an interplay between network architecture and dynamics, structure plays an important role in communication and spreading of information in a network. Here we investigate the underlying undirected topology of different biological networks which support faster spreading of information and are better in communication. We analyse the good expansion property by using the spectral gap and communicability between nodes. Different epidemic models are also used to study the transmission of information in terms of spreading of disease through individuals (nodes) in those networks. Moreover, we explore the structural conformation and properties which may be responsible for better communication. Among all biological networks studied here, the undirected structure of neuronal networks not only possesses the small-world property but the same is also expressed remarkably to a higher degree compared to any randomly generated network which possesses the same degree sequence. A relatively high percentage of nodes, in neuronal networks, form a higher core in their structure. Our study shows that the underlying undirected topology in neuronal networks, in a significant way, is qualitatively different from the same in other biological networks and that they may have evolved in such a way that they inherit a (undirected) structure which is excellent and robust in communication.     

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.     

Modular and hierarchical structure of social contact networks

Social contact networks exhibit overlapping qualities of communities, hierarchical structure and spatial-correlated nature. We propose a mixing pattern of modular and growing hierarchical structures to reconstruct social contact networks by using an individual’s geospatial distribution information in the real world. The hierarchical structure of social contact networks is defined based on the spatial distance between individuals, and edges among individuals are added in turn from the modular layer to the highest layer. It is a gradual process to construct the hierarchical structure: from the basic modular model up to the global network. The proposed model not only shows hierarchically increasing degree distribution and large clustering coefficients in communities, but also exhibits spatial clustering features of individual distributions. As an evaluation of the method, we reconstruct a hierarchical contact network based on the investigation data of a university. Transmission experiments of influenza H1N1 are carried out on the generated social contact networks, and results show that the constructed network is efficient to reproduce the dynamic process of an outbreak and evaluate interventions. The reproduced spread process exhibits that the spatial clustering of infection is accordant with the clustering of network topology. Moreover, the effect of individual topological character on the spread of influenza is analyzed, and the experiment results indicate that the spread is limited by individual daily contact patterns and local clustering topology rather than individual degree.     

Identifying an influential spreader from a single seed in complex networks via a message-passing approach

Identifying the most influential spreaders is one of outstanding problems in physics of complex systems. So far, many approaches have attempted to rank the influence of nodes but there is still the lack of accuracy to single out influential spreaders. Here, we directly tackle the problem of finding important spreaders by solving analytically the expected size of epidemic outbreaks when spreading originates from a single seed. We derive and validate a theory for calculating the size of epidemic outbreaks with a single seed using a message-passing approach. In addition, we find that the probability to occur epidemic outbreaks is highly dependent on the location of the seed but the size of epidemic outbreaks once it occurs is insensitive to the seed. We also show that our approach can be successfully adapted into weighted networks.     

Comparison of immunization strategies in geographical networks

The epidemic spread and immunizations in geographically embedded scale-free (SF) and Watts-Strogatz (WS) networks are numerically investigated. We make a realistic assumption that it takes time which we call the detection time, for a vertex to be identified as infected, and implement two different immunization strategies: one is based on connection neighbors (CN) of the infected vertex with the exact information of the network structure utilized and the other is based on spatial neighbors (SN) with only geographical distances taken into account. We find that the decrease of the detection time is crucial for a successful immunization in general. Simulation results show that for both SF networks and WS networks, the SN strategy always performs better than the CN strategy, especially for more heterogeneous SF networks at long detection time. The observation is verified by checking the number of the infected nodes being immunized. We found that in geographical space, the distance preferences in the network construction process and the geographically decaying infection rate are key factors that make the SN immunization strategy outperforms the CN strategy. It indicates that even in the absence of the full knowledge of network connectivity we can still stop the epidemic spread efficiently only by using geographical information as in the SN strategy, which may have potential applications for preventing the real epidemic spread.