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.     

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.     

The impact of awareness on epidemic spreading in networks

We explore the impact of awareness on epidemic spreading through a population represented by a scale-free network. Using a network mean-field approach, a mathematical model for epidemic spreading with awareness reactions is proposed and analyzed. We focus on the role of three forms of awareness including local, global, and contact awareness. By theoretical analysis and simulation, we show that the global awareness cannot decrease the likelihood of an epidemic outbreak while both the local awareness and the contact awareness can. Also, the influence degree of the local awareness on disease dynamics is closely related with the contact awareness.     

Magnetic and quantum entanglement properties of the distorted diamond chain model for azurite

On the basis of experimental data on interactions between humans we have investigated the process of epidemic spreading in a social network. We found that the distribution of the number of contacts maintained in one day is exponential. Data on frequency and duration of interpersonal interactions are presented. They allow us to simulate the spread of droplet-/-air-borne infections and to investigate the influence of human dynamics on the epidemic spread. Specifically, we investigated the influence of the distribution of frequency and duration of those contacts on magnitude, epidemic threshold and peak timing of epidemics propagating in respective networks. It turns out that a large increase in the magnitude of an epidemic and a decrease in epidemic threshold are visible if and only if both are taken into account. We have found that correlation between contact frequency and duration strongly influences the effectiveness of control measures like mass immunization campaigns.     

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.     

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.     

Unfolding proteins under external forces: a solvable model under the self-consistent pair contact probability approximation

We extend a model of Micheletti et al. [Phys. Rev. Lett. 87, 088102 (2001)]] used to study protein con-formations to the case in which there is an external force field. Under the self-consistent pair contact probability approximation, this residue-level resolution model can still be solved under pulling forces. We implement the algorithm using heterogeneous parameters and study the force-induced unfolding of a helical segment from the protein transformylase and of the beta-stranded domains from the protein titin. The results are qualitatively consistent with the results from more expensive, atomistic dynamics simulation. Despite the mean-field-like approach, we observed a sharp and cooperative unfolding transition.     

Proximity networks and epidemics

Disease spread in most biological populations requires the proximity of agents. In populations where the individuals have spatial mobility, the contact graph is generated by the “collision dynamics” of the agents, and thus the evolution of epidemics couples directly to the spatial dynamics of the population. We first briefly review the properties and the methodology of an agent-based simulation (EPISIMS) to model disease spread in realistic urban dynamic contact networks. Using the data generated by this simulation, we introduce the notion of dynamic proximity networks which takes into account the relevant time-scales for disease spread: contact duration, infectivity period, and rate of contact creation. This approach promises to be a good candidate for a unified treatment of epidemic types that are driven by agent collision dynamics. In particular, using a simple model, we show that it can account for the observed qualitative differences between the degree distributions of contact graphs of diseases with short infectivity period (such as air-transmitted diseases) or long infectivity periods (such as HIV).     

Synchronized cluster formation in coupled laser networks

We experimentally investigate the phase dynamics of laser networks with homogenous time-delayed mutual coupling and establish the fundamental rules that govern their state of synchronization. We identified a specific substructure that imposes its synchronization state on the entire network and show that for any coupling configuration the network forms at most two synchronized clusters. Our results indicate that the synchronization state of the network is a nonlocal phenomenon and cannot be deduced by decomposing the network into smaller substructures, each with its individual synchronization state.     

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     

Comparative effects of avoidance and vaccination in disease spread on a dynamic small-world network

Dynamic small-world contact networks have fixed short range links and time-varying stochastic long range links. They are used to model mobile populations or as minimal models for traditional small-world networks. Here we study the relative effects of vaccinations and avoidance of infected individuals in a susceptible-infected-recovered (SIR) epidemic model on a dynamic small-world network. We derive the critical mobility required for an outbreak to occur as a function of the disease’s infectivity, recovery rate, avoidance rate, and vaccination rate. We also derive an expression that allows us to calculate the amount of vaccination and/or avoidance necessary to prevent an epidemic. Calculated quantities show excellent agreement with simulations.     

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.     

Effects of City-Size Heterogeneity on Epidemic Spreading in a Metapopulation: A Reaction-Diffusion Approach

We review and introduce a generalized reaction-diffusion approach to epidemic spreading in a metapopulation modeled as a complex network. The metapopulation consists of susceptible and infected individuals that are grouped in subpopulations symbolizing cities and villages that are coupled by human travel in a transportation network. By analytic methods and numerical simulations we calculate the fraction of infected people in the metapopulation in the long time limit, as well as the relevant parameters characterizing the epidemic threshold that separates an epidemic from a non-epidemic phase. Within this model, we investigate the effect of a heterogeneous network topology and a heterogeneous subpopulation size distribution. Such a system is suited for epidemic modeling where small villages and big cities exist simultaneously in the metapopulation. We find that the heterogeneous conditions cause the epidemic threshold to be a non-trivial function of the reaction rates (local parameters), the network’s topology (global parameters) and the cross-over population size that separates “village dynamics” from “city dynamics”.     

Effect of incubation period on epidemic spreading in complex networks

We study the effect of incubation period on epidemic spreading in the Barabasi--Albert scale-free network and the Watts--Strogatz small world network by using a Suspectable-Incubated-Infected-Suspectable model. Our analytical investigations show that the epidemic threshold is independent of incubation period in both networks, which is verified by our large-scale simulation results. We also investigate the effect of incubation period on the epidemic dynamics in a supercritical regime. It is found that with the increase of incubation period Ω , a damped oscillation evolution of ρ_T(the ratio of persons in incubated state) appears and the time needed to reach a saturation value increases. Moreover, the steady value of ρ_T increases and approaches to an asymptotic constant with the value of {\it\Omega} increasing. As a result, the infected ratio ρ_I decreases with the increase of Ω according to a power law.     

Scaling of the propagation of epidemics in a system of mobile agents

For a two-dimensional system of agents modeled by molecular dynamics, we simulate epidemics spreading, which was recently studied on complex networks. Our resulting network model is time-evolving. We study the transitions to spreading as function of density, temperature and infection time. In addition, we analyze the epidemic threshold associated to a power-law distribution of infection times.     

Spreading processes on dynamically changing contact networks

We develop and analyze an agent-based model for the study of information propagation in dynamic contact networks. We represent information as a state of a node in a network that can be probabilistically transferred to an adjacent node within a single time step. The model is based on a closed (yet sufficiently large) population that can support processes of link generation and annihilation using different contact regimes. Our study is confined to the case of homogeneous contacts, where each agent establishes and breaks contacts in the same way. We consider information to be available for spreading in a fixed time window (i.e. finite memory). We find, surprisingly, that information transmission (measured as the proportion of informed nodes after a fixed number of time steps) is identical for dynamic preferential and random networks, but radically different for the associate mixing contact regime. We also find that the probability of transmission is, similarly counterintuitively, not a main driver of the process as opposed the the main network par maters determining contact lifetime and the turnover rate on connections. We discuss the explanation and the significance of these results in the light of the fundamental difference between dynamic and static (cumulative) networks.     

Stochastic epidemics and rumours on finite random networks

In this paper, we investigate the stochastic spread of epidemics and rumours on networks. We focus on the general stochastic (SIR) epidemic model and a recently proposed rumour model on networks in Nekovee et al. (2007) [3], and on networks with different random structures, taking into account the structure of the underlying network at the level of the degree–degree correlation function. Using embedded Markov chain techniques and ignoring density correlations between neighbouring nodes, we derive a set of equations for the final size of the epidemic/rumour on a homogeneous network that can be solved numerically, and compare the resulting distribution with the solution of the corresponding mean-field deterministic model. The final size distribution is found to switch from unimodal to bimodal form (indicating the possibility of substantial spread of the epidemic/rumour) at a threshold value that is higher than that for the deterministic model. However, the difference between the two thresholds decreases with the network size, n, following a n^−1/3 behaviour. We then compare results (obtained by Monte Carlo simulation) for the full stochastic model on a homogeneous network, including density correlations at neighbouring nodes, with those for the approximating stochastic model and show that the latter reproduces the exact simulation results with great accuracy. Finally, further Monte Carlo simulations of the full stochastic model are used to explore the effects on the final size distribution of network size and structure (using homogeneous networks, simple random graphs and the Barabasi–Albert scale-free networks).     

Effects of friend-making resources/costs and remembering on acquaintance networks

We consider two overlooked yet important factors that affect acquaintance network evolution and formation—friend-making resources and remembering—and propose a bottom-up, network-oriented simulation model based on three rules representing human social interactions. Our proposed model reproduces many topological features of real-world acquaintance networks, including a small-world phenomenon and a sharply peaked connectivity distribution feature that mixes power-law and exponential distribution types. We believe that this is an improvement over fieldwork sampling methods that fail to capture acquaintance network node connectivity distributions. Our model may produce valuable results for sociologists working with social opinion formation and epidemiologists studying epidemic dynamics.     

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.     

Strength distribution of novel local-world networks

It is discovered that there are two important characters, local-world character and weight-driven character, in many real-life complex networks. Motivated by this fact, a weight-driven local-world network model is proposed, which incorporates the weight dynamics and the fixed local-world property. By means of mathematical analysis and numerical simulation, the strength distribution of the network model has been obtained. The results are applied to epidemic spreading theory.