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Register a new userThe hidden dependence of spreading vulnerability on topological complexity
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Many dynamical phenomena, e.g., pathogen transmission, disruptions in transport over networks, and (fake) news purveyance, concern spreading that plays out on top of networks with changing architectures over time - commonly known as temporal networks. Assessing a systems proneness to facilitate spreading phenomena, which we refer to as its spreading vulnerability, from its topological information alone remains a challenging task. We report a methodological advance in terms of a novel metric for topological complexity: entanglement entropy. Using publicly available datasets, we demonstrate that the metric naturally allows for topological comparisons across vastly different systems, and importantly, reveals that the spreading vulnerability of a system can be quantitatively related to its topological complexity. In doing so, the metric opens itself for applications in a wide variety of natural, social, biological and engineered systems.
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Computer viruses are evolving by developing spreading mechanisms based on the use of multiple vectors of propagation. The use of the social network as an extra vector of attack to penetrate the security measures in IP networks is improving the effectiveness of malware, and have therefore been used by the most aggressive viruses, like Conficker and Stuxnet. In this work we use interdependent networks to model the propagation of these kind of viruses. In particular, we study the propagation of a SIS model on interdependent networks where the state of each node is layer-independent and the dynamics in each network follows either a contact process or a reactive process, with different propagation rates. We apply this study to the case of existing multilayer networks, namely a Spanish scientific community of Statistical Physics, formed by a social network of scientific collaborations and a physical network of connected computers in each institution. We show that the interplay between layers increases dramatically the infectivity of viruses in the long term and their robustness against immunization.
Social interactions are stratified in multiple contexts and are subject to complex temporal dynamics. The systematic study of these two features of social systems has started only very recently mainly thanks to the development of multiplex and time-varying networks. However, these two advancements have progressed almost in parallel with very little overlap. Thus, the interplay between multiplexity and the temporal nature of connectivity patterns is poorly understood. Here, we aim to tackle this limitation by introducing a time-varying model of multiplex networks. We are interested in characterizing how these two properties affect contagion processes. To this end, we study SIS epidemic models unfolding at comparable time-scale respect to the evolution of the multiplex network. We study both analytically and numerically the epidemic threshold as a function of the overlap between, and the features of, each layer. We found that, the overlap between layers significantly reduces the epidemic threshold especially when the temporal activation patterns of overlapping nodes are positively correlated. Furthermore, when the average connectivity across layers is very different, the contagion dynamics are driven by the features of the more densely connected layer. Here, the epidemic threshold is equivalent to that of a single layered graph and the impact of the disease, in the layer driving the contagion, is independent of the overlap. However, this is not the case in the other layers where the spreading dynamics are sharply influenced by it. The results presented provide another step towards the characterization of the properties of real networks and their effects on contagion phenomena
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.
Online social media have greatly affected the way in which we communicate with each other. However, little is known about what are the fundamental mechanisms driving dynamical information flow in online social systems. Here, we introduce a generative model for online sharing behavior that is analytically tractable and which can reproduce several characteristics of empirical micro-blogging data on hashtag usage, such as (time-dependent) heavy-tailed distributions of meme popularity. The presented framework constitutes a null model for social spreading phenomena which, in contrast to purely empirical studies or simulation-based models, clearly distinguishes the roles of two distinct factors affecting meme popularity: the memory time of users and the connectivity structure of the social network.
Background: Controlling global epidemics in the real world and accelerating information propagation in the artificial world are of great significance, which have activated an upsurge in the studies on networked spreading dynamics. Lots of efforts have been made to understand the impacts of macroscopic statistics (e.g., degree distribution and average distance) and mesoscopic structures (e.g., communities and rich clubs) on spreading processes while the microscopic elements are less concerned. In particular, roles of ties are not yet clear to the academic community. Methodology/Principle Findings: Every edges is stamped by its strength that is defined solely based on the local topology. According to a weighted susceptible-infected-susceptible model, the steady-state infected density and spreading speed are respectively optimized by adjusting the relationship between edges strength and spreading ability. Experiments on six real networks show that the infected density is increased when strong ties are favored in the spreading, while the speed is enhanced when weak ties are favored. Significance of these findings is further demonstrated by comparing with a null model. Conclusions/Significance: Experimental results indicate that strong and weak ties play distinguishable roles in spreading dynamics: the former enlarge the infected density while the latter fasten the process. The proposed method provides a quantitative way to reveal the qualitatively different roles of ties, which could find applications in analyzing many networked dynamical processes with multiple performance indices, such as synchronizability and converging time in synchronization and throughput and delivering time in transportation.
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