1,113 research outputs found

    A framework for epidemic spreading in multiplex networks of metapopulations

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    We propose a theoretical framework for the study of epidemics in structured metapopulations, with heterogeneous agents, subjected to recurrent mobility patterns. We propose to represent the heterogeneity in the composition of the metapopulations as layers in a multiplex network, where nodes would correspond to geographical areas and layers account for the mobility patterns of agents of the same class. We analyze both the classical Susceptible-Infected-Susceptible and the Susceptible-Infected-Removed epidemic models within this framework, and compare macroscopic and microscopic indicators of the spreading process with extensive Monte Carlo simulations. Our results are in excellent agreement with the simulations. We also derive an exact expression of the epidemic threshold on this general framework revealing a non-trivial dependence on the mobility parameter. Finally, we use this new formalism to address the spread of diseases in real cities, specifically in the city of Medellin, Colombia, whose population is divided into six socio-economic classes, each one identified with a layer in this multiplex formalism.Comment: 13 pages, 11 figure

    Social contagions on interdependent lattice networks

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    Although an increasing amount of research is being done on the dynamical processes on interdependent spatial networks, knowledge of how interdependent spatial networks influence the dynamics of social contagion in them is sparse. Here we present a novel non-Markovian social contagion model on interdependent spatial networks composed of two identical two-dimensional lattices. We compare the dynamics of social contagion on networks with different fractions of dependency links and find that the density of final recovered nodes increases as the number of dependency links is increased. We use a finite-size analysis method to identify the type of phase transition in the giant connected components (GCC) of the final adopted nodes and find that as we increase the fraction of dependency links, the phase transition switches from second-order to first-order. In strong interdependent spatial networks with abundant dependency links, increasing the fraction of initial adopted nodes can induce the switch from a first-order to second-order phase transition associated with social contagion dynamics. In networks with a small number of dependency links, the phase transition remains second-order. In addition, both the second-order and first-order phase transition points can be decreased by increasing the fraction of dependency links or the number of initially-adopted nodes.This work was partially supported by National Natural Science Foundation of China (Grant Nos 61501358, 61673085), and the Fundamental Research Funds for the Central Universities. (61501358 - National Natural Science Foundation of China; 61673085 - National Natural Science Foundation of China; Fundamental Research Funds for the Central Universities)Published versio

    Spreading processes in Multilayer Networks

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    Several systems can be modeled as sets of interconnected networks or networks with multiple types of connections, here generally called multilayer networks. Spreading processes such as information propagation among users of an online social networks, or the diffusion of pathogens among individuals through their contact network, are fundamental phenomena occurring in these networks. However, while information diffusion in single networks has received considerable attention from various disciplines for over a decade, spreading processes in multilayer networks is still a young research area presenting many challenging research issues. In this paper we review the main models, results and applications of multilayer spreading processes and discuss some promising research directions.Comment: 21 pages, 3 figures, 4 table

    Disease Localization in Multilayer Networks

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    We present a continuous formulation of epidemic spreading on multilayer networks using a tensorial representation, extending the models of monoplex networks to this context. We derive analytical expressions for the epidemic threshold of the SIS and SIR dynamics, as well as upper and lower bounds for the disease prevalence in the steady state for the SIS scenario. Using the quasi-stationary state method we numerically show the existence of disease localization and the emergence of two or more susceptibility peaks, which are characterized analytically and numerically through the inverse participation ratio. Furthermore, when mapping the critical dynamics to an eigenvalue problem, we observe a characteristic transition in the eigenvalue spectra of the supra-contact tensor as a function of the ratio of two spreading rates: if the rate at which the disease spreads within a layer is comparable to the spreading rate across layers, the individual spectra of each layer merge with the coupling between layers. Finally, we verified the barrier effect, i.e., for three-layer configuration, when the layer with the largest eigenvalue is located at the center of the line, it can effectively act as a barrier to the disease. The formalism introduced here provides a unifying mathematical approach to disease contagion in multiplex systems opening new possibilities for the study of spreading processes.Comment: Revised version. 25 pages and 18 figure

    Competing contagion processes: Complex contagion triggered by simple contagion

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    Empirical evidence reveals that contagion processes often occur with competition of simple and complex contagion, meaning that while some agents follow simple contagion, others follow complex contagion. Simple contagion refers to spreading processes induced by a single exposure to a contagious entity while complex contagion demands multiple exposures for transmission. Inspired by this observation, we propose a model of contagion dynamics with a transmission probability that initiates a process of complex contagion. With this probability nodes subject to simple contagion get adopted and trigger a process of complex contagion. We obtain a phase diagram in the parameter space of the transmission probability and the fraction of nodes subject to complex contagion. Our contagion model exhibits a rich variety of phase transitions such as continuous, discontinuous, and hybrid phase transitions, criticality, tricriticality, and double transitions. In particular, we find a double phase transition showing a continuous transition and a following discontinuous transition in the density of adopted nodes with respect to the transmission probability. We show that the double transition occurs with an intermediate phase in which nodes following simple contagion become adopted but nodes with complex contagion remain susceptible.Comment: 9 pages, 4 figure
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