1,113 research outputs found
A framework for epidemic spreading in multiplex networks of metapopulations
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
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
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
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
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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