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Register a new userSuppressing traffic-driven epidemic spreading by edge-removal strategies
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The interplay between traffic dynamics and epidemic spreading on complex networks has received increasing attention in recent years. However, the control of traffic-driven epidemic spreading remains to be a challenging problem. In this Brief Report, we propose a method to suppress traffic-driven epidemic outbreak by properly removing some edges in a network. We find that the epidemic threshold can be enhanced by the targeted cutting of links among large-degree nodes or edges with the largest algorithmic betweeness. In contrast, the epidemic threshold will be reduced by the random edge removal. These findings are robust with respect to traffic-flow conditions, network structures and routing strategies. Moreover, we find that the shutdown of targeted edges can effectively release traffic load passing through large-degree nodes, rendering a relatively low probability of infection to these nodes.
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Despite extensive work on the interplay between traffic dynamics and epidemic spreading, the control of epidemic spreading by routing strategies has not received adequate attention. In this paper, we study the impact of efficient routing protocol on epidemic spreading. In the case of infinite node-delivery capacity, where the traffic is free of congestion, we find that that there exists optimal values of routing parameter, leading to the maximal epidemic threshold. This means that epidemic spreading can be effectively controlled by fine tuning the routing scheme. Moreover, we find that an increase in the average network connectivity and the emergence of traffic congestion can suppress the epidemic outbreak.
In spite of the extensive previous efforts on traffic dynamics and epidemic spreading in complex networks, the problem of traffic-driven epidemic spreading on {em correlated} networks has not been addressed. Interestingly, we find that the epidemic threshold, a fundamental quantity underlying the spreading dynamics, exhibits a non-monotonic behavior in that it can be minimized for some critical value of the assortativity coefficient, a parameter characterizing the network correlation. To understand this phenomenon, we use the degree-based mean-field theory to calculate the traffic-driven epidemic threshold for correlated networks. The theory predicts that the threshold is inversely proportional to the packet-generation rate and the largest eigenvalue of the betweenness matrix. We obtain consistency between theory and numerics. Our results may provide insights into the important problem of controlling/harnessing real-world epidemic spreading dynamics driven by traffic flows.
We study SIS epidemic spreading processes unfolding on a recent generalisation of the activity-driven modelling framework. In this model of time-varying networks each node is described by two variables: activity and attractiveness. The first, describes the propensity to form connections. The second, defines the propensity to attract them. We derive analytically the epidemic threshold considering the timescale driving the evolution of contacts and the contagion as comparable. The solutions are general and hold for any joint distribution of activity and attractiveness. The theoretical picture is confirmed via large-scale numerical simulations performed considering heterogeneous distributions and different correlations between the two variables. We find that heterogeneous distributions of attractiveness alter the contagion process. In particular, in case of uncorrelated and positive correlations between the two variables, heterogeneous attractiveness facilitates the spreading. On the contrary, negative correlations between activity and attractiveness hamper the spreading. The results presented contribute to the understanding of the dynamical properties of time-varying networks and their effects on contagion phenomena unfolding on their fabric.
The study of complex networks sheds light on the relation between the structure and function of complex systems. One remarkable result is the absence of an epidemic threshold in infinite-size scale-free networks, which implies that any infection will perpetually propagate regardless of the spreading rate. The vast majority of current theoretical approaches assumes that infections are transmitted as a reaction process from nodes to all neighbors. Here we adopt a different perspective and show that the epidemic incidence is shaped by traffic flow conditions. Specifically, we consider the scenario in which epidemic pathways are defined and driven by flows. Through extensive numerical simulations and theoretical predictions, it is shown that the value of the epidemic threshold in scale-free networks depends directly on flow conditions, in particular on the first and second moments of the betweenness distribution given a routing protocol. We consider the scenarios in which the delivery capability of the nodes is bounded or unbounded. In both cases, the threshold values depend on the traffic and decrease as flow increases. Bounded delivery provokes the emergence of congestion, slowing down the spreading of the disease and setting a limit for the epidemic incidence. Our results provide a general conceptual framework to understand spreading processes on complex networks.
Although suppressing the spread of a disease is usually achieved by investing in public resources, in the real world only a small percentage of the population have access to government assistance when there is an outbreak, and most must rely on resources from family or friends. We study the dynamics of disease spreading in social-contact multiplex networks when the recovery of infected nodes depends on resources from healthy neighbors in the social layer. We investigate how degree heterogeneity affects the spreading dynamics. Using theoretical analysis and simulations we find that degree heterogeneity promotes disease spreading. The phase transition of the infected density is hybrid and increases smoothly from zero to a finite small value at the first invasion threshold and then suddenly jumps at the second invasion threshold. We also find a hysteresis loop in the transition of the infected density. We further investigate how an overlap in the edges between two layers affects the spreading dynamics. We find that when the amount of overlap is smaller than a critical value the phase transition is hybrid and there is a hysteresis loop, otherwise the phase transition is continuous and the hysteresis loop vanishes. In addition, the edge overlap allows an epidemic outbreak when the transmission rate is below the first invasion threshold, but suppresses any explosive transition when the transmission rate is above the first invasion threshold.
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