Threshold effects for two pathogens spreading on a network

Diseases spread through host populations over the networks of contacts between individuals and a number of results about this process have been derived in recent years by exploiting connections between epidemic processes and bond percolation on networks. Here we investigate the case of two pathogens in a single population, which has been the subject of recent interest among epidemiologists. We demonstrate that two pathogens competing for the same hosts can both spread through a population only for intermediate values of the bond occupation probability that lie above the classic epidemic threshold and below a second higher value, which we call the coexistence threshold, corresponding to a distinct topological phase transition in networked systems.     

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.     

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.     

Effect of structural features on the thermal conductivity of SiGe-based materials

On the basis of the experimental data concerning interactions between humans the process of epidemic spreading in a social network was investigated. It was found that number of contact and average age of nearest neighbors are highly correlated with age of an individual. The influence of those correlations on the process of epidemic spreading and effectiveness of control measures like mass immunizations campaigns was investigated. It occurs that the magnitude of epidemic is decreased and the effectiveness of target vaccination is increased.     

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 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.     

Scaling behavior of threshold epidemics

We study the classic Susceptible-Infected-Recovered (SIR) model for the spread of an infectious disease. In this stochastic process, there are two competing mechanism: infection and recovery. Susceptible individuals may contract the disease from infected individuals, while infected ones recover from the disease at a constant rate and are never infected again. Our focus is the behavior at the epidemic threshold where the rates of the infection and recovery processes balance. In the infinite population limit, we establish analytically scaling rules for the time-dependent distribution functions that characterize the sizes of the infected and the recovered sub-populations. Using heuristic arguments, we also obtain scaling laws for the size and duration of the epidemic outbreaks as a function of the total population. We perform numerical simulations to verify the scaling predictions and discuss the consequences of these scaling laws for near-threshold epidemic outbreaks.     

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.     

Epidemic spreading in communities with mobile agents

We propose a model of mobile agents to study the epidemic spreading in communities with different densities of agents, which aims to simulate the realistic situation of multiple cities. The model addresses the epidemic process from a community with threshold λ_c1 less than the infection rate λ to a community with threshold λ_c2 larger than λ through both direct and indirect contacts. By both theoretic analysis and numerical simulations we show that it is possible to sustain the epidemic spreading in the community with λ_c2 through contact with another community, provided that the latter is connected with an infected community. This result suggests that for effectively controlling the epidemic spread, we should also pay attention to the risk caused by the infection through indirect contact.     

Crossover from weak to strong disorder regime in the duration of epidemics

We study the susceptible–infected–recovered (SIR) model in complex networks, considering that not all individuals in the population interact in the same way. This heterogeneity between contacts is modeled by a continuous disorder. In our model, the disorder represents the contact time or the closeness between individuals. We find that the duration time of an epidemic has a crossover with the system size, from a power-law regime to a logarithmic regime depending on the transmissibility related to the strength of the disorder. Using percolation theory, we find that the duration of the epidemic scales as the average length of the branches of the infection. Our theoretical findings, supported by simulations, explains the crossover between the two regimes.     

SIR model of epidemic spread with accumulated exposure

We study an extended and modified SIR model of epidemic spread in which susceptible agents during interactions with infectious neighbors are exposed to the disease and can consequently become infectious. The studied model is extended to include heterogeneity of interactions which is modelled assuming random character of the dose accumulated by susceptible agents in every interaction with infectious neighbors. When the accumulated exposure is larger than the individual’s resistance, an agent becomes infectious and consequently introduces a new source of an epidemic which is capable of passing the disease further. We study statistical properties characterizing the course of an epidemic. The examination of the modified SIR model reveals a possible “resonant activation”-like behavior of the system in the duration of the epidemic outbreak and a possible bistable behavior of the model with accumulated exposure. Furthermore, the linear scaling of the duration of the epidemic with the system size for a wide range of the model parameters is recorded.     

Modelling temporal networks of human face-to-face contacts with public activity and individual reachability

Modelling temporal networks of human face-to-face contacts is vital both for understanding the spread of airborne pathogens and word-of-mouth spreading of information. Although many efforts have been devoted to model these temporal networks, there are still two important social features, public activity and individual reachability, have been ignored in these models. Here we present a simple model that captures these two features and other typical properties of empirical face-to-face contact networks. The model describes agents which are characterized by an attractiveness to slow down the motion of nearby people, have event-triggered active probability and perform an activity-dependent biased random walk in a square box with periodic boundary. The model quantitatively reproduces two empirical temporal networks of human face-to-face contacts which are testified by their network properties and the epidemic spread dynamics on them.     

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.     

Modelling of discrete-time SIS models with awareness interactions on degree-uncorrelated networks

Many epidemic models ignored the impact of awareness on epidemics in a population, though it is not the case from the real viewpoints. In this paper, a discrete-time SIS model with awareness interactions on degree-uncorrelated networks is considered. We study three kinds of awareness, including local awareness and global awareness which are originated from the epidemic-dependent information, and individual awareness which is epidemic-independent and determined by the individual information. We demonstrate analytically that awareness of the epidemic-dependent information cannot change the epidemic threshold regardless of the global or local spreading information. In contrast, epidemic-independent awareness to individual information increases the epidemic threshold in finite scale-free networks, but cannot halt the absence of epidemic threshold in an infinite scale-free network. By numerical simulations, we find that local awareness has a stronger impact on epidemic prevalence than global awareness. Our findings explore the effects of various types of awareness on epidemic spreading and address their roles in the epidemic control.     

无标度网络中最大传染能力限定的病毒传播问题研究

传统的病毒传播模型在无限大无标度网络上不存在病毒传播阈值,即无论病毒的传播速率多么低,病毒始终能够在网络中传播.但研究发现,这个结论是在网络中存在超级传染者的假设下得到的,然而许多真实的无标度网络中并不存在超级传染者.因此,文章提出了一个最大传染能力限定的病毒传播模型,并从理论上证明了在最大传染能力限定的无限大无标度网络上,病毒传播阈值是存在的;同时,也分析了最大传染能力限定下非零传播阈值与有限规模网络下非零传播阈值的本质区别,并解释了为什么人们总是认为传统病毒传播模型对许多真实网络病毒感染程度估计过高的 关键词： 无标度网络 最大传染能力 传播阈值 感染程度     

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.     

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.     

Effects of delayed recovery and nonuniform transmission on the spreading of diseases in complex networks

We investigate the effects of delaying the time to recovery (delayed recovery) and of nonuniform transmission on the propagation of diseases on structured populations. Through a mean-field approximation and large-scale numerical simulations, we find that postponing the transition from the infectious to the recovered states can largely reduce the epidemic threshold, therefore promoting the outbreak of epidemics. On the other hand, if we consider nonuniform transmission among individuals, the epidemic threshold increases, thus inhibiting the spreading process. When both mechanisms are at work, the latter might prevail, hence resulting in an increase of the epidemic threshold with respect to the standard case, in which both ingredients are absent. Our findings are of interest for a better understanding of how diseases propagate on structured populations and to a further design of efficient immunization strategies.     

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).