اشترك بالحزمة الذهبية واحصل على وصول غير محدود شمرا أكاديميا
تسجيل مستخدم جديدTraffic-driven epidemic spreading in correlated networks
165
0
0.0
(
0
)
اسأل ChatGPT حول البحث
ﻻ يوجد ملخص باللغة العربية
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.
قيم البحث
اقرأ أيضاً
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, describ
es 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.
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.
We investigate the effect of degree correlation on a susceptible-infected-susceptible (SIS) model with a nonlinear cooperative effect (synergy) in infectious transmissions. In a mean-field treatment of the synergistic SIS model on a bimodal network w
ith tunable degree correlation, we identify a discontinuous transition that is independent of the degree correlation strength unless the synergy is absent or extremely weak. Regardless of synergy (absent or present), a positive and negative degree correlation in the model reduces and raises the epidemic threshold, respectively. For networks with a strongly positive degree correlation, the mean-field treatment predicts the emergence of two discontinuous jumps in the steady-state infected density. To test the mean-field treatment, we provide approximate master equations of the present model, which accurately describe the synergistic SIS dynamics. We quantitatively confirm all qualitative predictions of the mean-field treatment in numerical evaluations of the approximate master equations.
سجل دخول لتتمكن من نشر تعليقات
التعليقات
جاري جلب التعليقات
سجل دخول لتتمكن من متابعة معايير البحث التي قمت باختيارها
