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Register a new userTraffic-driven Epidemic Spreading in Finite-size Scale-Free Networks
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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.
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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.
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.
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.
We give an intuitive though general explanation of the finite-size effect in scale-free networks in terms of the degree distribution of the starting network. This result clarifies the relevance of the starting network in the final degree distribution. We use two different approaches: the deterministic mean-field approximation used by Barabasi and Albert (but taking into account the nodes of the starting network), and the probability distribution of the degree of each node, which considers the stochastic process. Numerical simulations show that the accuracy of the predictions of the mean-field approximation depend on the contribution of the dispersion in the final distribution. The results in terms of the probability distribution of the degree of each node are very accurate when compared to numerical simulations. The analysis of the standard deviation of the degree distribution allows us to assess the influence of the starting core when fitting the model to real data.
A model for epidemic spreading on rewiring networks is introduced and analyzed for the case of scale free steady state networks. It is found that contrary to what one would have naively expected, the rewiring process typically tends to suppress epidemic spreading. In particular it is found that as in static networks, rewiring networks with degree distribution exponent $gamma >3$ exhibit a threshold in the infection rate below which epidemics die out in the steady state. However the threshold is higher in the rewiring case. For $2<gamma leq 3$ no such threshold exists, but for small infection rate the steady state density of infected nodes (prevalence) is smaller for rewiring networks.
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