复杂网络病毒传播的局域控制研究

从复杂网络的节点路径长度范围的角度来研究病毒传播的局域控制，分析了在不同拓扑结构的复杂网络中进行局域控制的有效性.研究表明，局域控制对WS小世界网络、BA无标度网络和ER随机网络三类复杂网络均有效，但只有WS小世界网络存在零感染的控制范围最优值d=3；对于长程连边的分布存在距离偏好的Kleinberg小世界网络，随着依赖度的增大，病毒传播率临界值增加，同时局域范围控制的效果得到加强. 关键词： 复杂网络 病毒传播 局域控制 路径长度     

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。     

基于一维元胞自动机的复杂网络恶意软件传播研究

基于一维元胞自动机,研究复杂网络恶意软件传播行为.利用信息网络节点全局交互的特点,建立元胞自动机邻域和状态转换函数,提出恶意软件传播模型,研究在多种网络拓扑下恶意软件传播的概率行为.研究表明,该模型能够准确描述在最近邻耦合网络（nearest-neighbor coupled network, NC）,Erdos-Renyi（ER）随机网络,Watts-Strogatz（WS） 小世界网络和Barabasi-Albert（BA）幂率网络等拓扑下的传播动力学行为,不仅能反映恶意软件传播的平均趋势,而且可以描述病毒消亡和渗透等稀有概率事件,有效克服基于平均场方法建立的微分方程模型只能反映传播的平均趋势,只适合对传播作整体预测的局限性.同时,研究指出网络中度分布的异质化程度和网络的局域空间交互特征是影响传播及免疫行为的关键要素. 关键词： 复杂网络 恶意软件传播 元胞自动机 状态转换函数     

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.     

基于感知流量算法的复杂网络拥塞问题研究

研究了在具有感知流量的路由策略下,复杂网络的拓扑结构对网络中传输流量的影响.为了描述数据包传输过程的有效性,通过引入一个状态参数,利用由稳态到拥塞的指标流量相变值来刻画网络的吞吐量.基于每个节点的数据包处理能力与该节点的度或介数成比例提出两种模型并进行仿真.仿真结果表明,平均度相同的情况下,模型Ⅰ中,WS小世界网络比ER随机网络和BA无标度网络更容易产生拥塞;模型Ⅱ中,所有网络容量都得到较大的提高,尤其是WS小世界网络.但当网络的基本连接参数改变时,哪种模型更利于网络的流量传输,还要依据网络本身的结构特性 关键词： 复杂网络 无标度网络 感知流量 拥塞     

识别高阶网络传播中最有影响力的节点

识别网络传播中最有影响力的节点是控制传播速度和范围的重要步骤,有助于加速有益信息扩散,抑制流行病、谣言和虚假信息的传播等.已有研究主要基于描述点对交互的低阶复杂网络.然而,现实中个体间的交互不仅发生在点对之间,也发生在3个及以上节点形成的群体中.群体交互可利用高阶网络来刻画,如单纯复形与超图.本文研究单纯复形上最有影响力的传播者识别方法.首先,提出单纯复形上易感-感染-恢复(SIR)微观马尔可夫链方程组,定量刻画单纯复形上的疾病传播动力学.接下来利用微观马尔可夫链方程组计算传播动力学中节点被感染的概率.基于网络结构与传播过程,定义节点的传播中心性,用于排序节点传播影响力.在两类合成单纯复形与4个真实单纯复形上的仿真结果表明,相比于现有高阶网络中心性和复杂网络中最优的中心性指标,本文提出的传播中心性能更准确地识别高阶网络中最有影响力的传播者.     

基于时滞耦合映像格子的多耦合边耦合网络级联抗毁性研究

现实中各网络之间的耦合促进了网络间的交流,但也带来了级联故障大范围传播的风险.考虑到故障的传播一般存在时滞,并且一个节点可能拥有不止一条耦合边的情况,本文构建了基于时滞耦合映像格子的多耦合边无标度耦合网络级联故障模型.研究表明,对于BA(Barabási-Albert)无标度耦合网络,存在一个阈值hT≈3,当耦合强度小于此阈值时,耦合越强抗毁性越弱;反之,耦合越强抗毁性反而越强.另外,研究发现时滞对耦合网络的影响不仅仅是延长了故障传播的时间,为采取防护措施争取了时间,而且也对最终故障规模产生了影响,具体地,当层内时滞τ1和层间时滞τ2可取任意值时,当两者成整数倍关系时其最终故障规模将更大.本文的研究可为构建高抗毁性的耦合网络或提高耦合网络的级联抗毁性提供参考.     

一个复杂网络家族的结构与同步能力研究

研究了一个介于BA无标度网络和ER随机网络之间的复杂网络家族的结构与同步能力。结果表明,在平均度保持不变的情况下,随着随机连接概率的增大,该网络家族的度分布趋于均匀,平均最短距离缓慢增大,簇系数缓慢减小,对于同步稳定区域无界的动力学系统,网络家族的同步能力基本保持不变,而对于同步稳定区域有界的动力学系统,网络家族的同步能力则逐步提高,并与度分布的标准差成线性关系。有助于理解网络结构对同步能力的影响,且对如何提高网络的同步能力有一定的指导意义。     

复杂网络的顶点着色及其在疾病免疫中的应用

在复杂网络研究中, 对于网络结构特征的分析已经引起了人们的极大关注, 而其中的网络着色问题却没有得到足够的重视. 为了理解网络结构与着色之间的关系, 本文研究了WS, BA网络以及不同宏观结构参量对于正常K色数的影响, 发现最大团数可以大致反映正常K色数的变化趋势, 而网络的平均度和匹配系数比异质性和聚类系数对于色数的影响更大. 对于一些实际网络的正常着色验证了本文的分析结果. 对复杂网络的顶点进行着色后, 根据独立集内任意两个顶点均不相邻的特点, 我们提出了基于独立集的免疫策略. 与全网随机免疫相比, 基于独立集的免疫策略可令网络更为脆弱, 从而有效抑制疾病的传播. 基于网络着色的独立集提供了一种崭新的免疫思路, 作为一个简单而适用的平台,有助于设计更为有效的免疫策略. 关键词： 复杂网络 正常着色 独立集 免疫策略     

传播过程中出现双峰现象的原因分析

最近二十年来科学家深入研究了与复杂网络相关的各种问题,在网络结构与同步、博弈、传播等动力学的相互作用方面取得了巨大的研究进展。目前人们已经对网络上的传播问题有了深入的了解,但对具体的传播过程考察的还不够深入。本文以疾病传播过程中的双峰现象为研究对象,主要考察感染率、群落的不同平均度和群落间连边数量这三个因素对双峰现象的影响。研究结果表明:群落或多层结构是产生双峰现象的必要条件,并且当感染率大于传播阈值时,群落或多层结构越明显,越容易观察到双峰现象;当群落结构或多层结构比较明显时,即使是结构相似的两个群落,当它们的平均度差别不大时,只要感染率大于传播阈值就能观察到双峰现象。我们的工作进一步明确了影响传播双峰现象的主要因素,加深了人们对网络结构因素和传播因素对同步过程的影响的认识。     

Epidemic spreading on weighted complex networks

Nowadays, the emergence of online services provides various multi-relation information to support the comprehensive understanding of the epidemic spreading process. In this Letter, we consider the edge weights to represent such multi-role relations. In addition, we perform detailed analysis of two representative metrics, outbreak threshold and epidemic prevalence, on SIS and SIR models. Both theoretical and simulation results find good agreements with each other. Furthermore, experiments show that, on fully mixed networks, the weight distribution on edges would not affect the epidemic results once the average weight of whole network is fixed. This work may shed some light on the in-depth understanding of epidemic spreading on multi-relation and weighted networks.     

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.     

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     

Modeling the COVID-19 epidemic and awareness diffusion on multiplex networks

The coronavirus disease 2019(COVID-19)has been widely spread around the world,and the control and behavior dynamics are still one of the important research directions in the world.Based on the characteristics of COVID-19’s spread,a coupled disease-awareness model on multiplex networks is proposed in this paper to study and simulate the interaction between the spreading behavior of COVID-19 and related information.In the layer of epidemic spreading,the nodes can be divided into five categories,where the topology of the network represents the physical contact relationship of the population.The topological structure of the upper network shows the information interaction among the nodes,which can be divided into aware and unaware states.Awareness will make people play a positive role in preventing the epidemic diffusion,influencing the spread of the disease.Based on the above model,we have established the state transition equation,through the microscopic Markov chain approach(MMCA),and proposed the propagation threshold calculation method under the epidemic model.Furthermore,MMCA iteration and the Monte Carlo method are simulated on the static network and dynamic network,respectively.The current results will be beneficial to the study of COVID-19,and propose a more rational and effective model for future research on epidemics.     

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 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.     

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.     

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.     

Imperfect targeted immunization in scale-free networks

Scale-free networks are prone to epidemic spreading. To provide cost-effective protection for such networks, targeted immunization was proposed to selectively immunize the hub nodes. In many real-life applications, however, the targeted immunization may not be perfect, either because some hub nodes are hidden and consequently not immunized, or because the vaccination simply cannot provide perfect protection. We investigate the effects of imperfect targeted immunization in scale-free networks. Analysis and simulation results show that there exists a linear relationship between the inverse of the epidemic threshold and the effectiveness of targeted immunization. Therefore, the probability of epidemic outbreak cannot be significantly lowered unless the protection is reasonably strong. On the other hand, even a relatively weak protection over the hub nodes significantly decreases the number of network nodes ever getting infected and therefore enhances network robustness against virus. We show that the above conclusions remain valid where there exists a negative correlation between nodal degree and infectiousness.