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Register a new userRoles of the spreading scope and effectiveness in spreading dynamics on multiplex networks
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Comparing with single networks, the multiplex networks bring two main effects on the spreading process among individuals. First, the pathogen or information can be transmitted to more individuals through different layers at one time, which enlarges the spreading scope. Second, through different layers, an individual can also transmit the pathogen or information to the same individuals more than once at one time, which makes the spreading more effective. To understand the different roles of the spreading scope and effectiveness, we propose an epidemic model on multiplex networks with link overlapping, where the spreading effectiveness of each interaction as well as the variety of channels (spreading scope) can be controlled by the number of overlapping links. We find that for Poisson degree distribution, increasing the epidemic scope (the first effect) is more efficient than enhancing epidemic probability (the second effect) to facilitate the spreading process. However, for power-law degree distribution, the effects of the two factors on the spreading dynamics become complicated. Enhancing epidemic probability makes pathogen or rumor easier to outbreak in a finite system. But after that increasing epidemic scopes is still more effective for a wide spreading. Theoretical results along with reasonable explanation for these phenomena are all given in this paper, which indicates that the epidemic scope could play an important role in the spreading dynamics.
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We introduce the sandpile model on multiplex networks with more than one type of edge and investigate its scaling and dynamical behaviors. We find that the introduction of multiplexity does not alter the scaling behavior of avalanche dynamics; the system is critical with an asymptotic power-law avalanche size distribution with an exponent $tau = 3/2$ on duplex random networks. The detailed cascade dynamics, however, is affected by the multiplex coupling. For example, higher-degree nodes such as hubs in scale-free networks fail more often in the multiplex dynamics than in the simplex network counterpart in which different types of edges are simply aggregated. Our results suggest that multiplex modeling would be necessary in order to gain a better understanding of cascading failure phenomena of real-world multiplex complex systems, such as the global economic crisis.
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
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.
Although there is always an interplay between the dynamics of information diffusion and disease spreading, the empirical research on the systemic coevolution mechanisms connecting these two spreading dynamics is still lacking. Here we investigate the coevolution mechanisms and dynamics between information and disease spreading by utilizing real data and a proposed spreading model on multiplex network. Our empirical analysis finds asymmetrical interactions between the information and disease spreading dynamics. Our results obtained from both the theoretical framework and extensive stochastic numerical simulations suggest that an information outbreak can be triggered in a communication network by its own spreading dynamics or by a disease outbreak on a contact network, but that the disease threshold is not affected by information spreading. Our key finding is that there is an optimal information transmission rate that markedly suppresses the disease spreading. We find that the time evolution of the dynamics in the proposed model qualitatively agrees with the real-world spreading processes at the optimal information transmission rate.
Although suppressing the spread of a disease is usually achieved by investing in public resources, in the real world only a small percentage of the population have access to government assistance when there is an outbreak, and most must rely on resources from family or friends. We study the dynamics of disease spreading in social-contact multiplex networks when the recovery of infected nodes depends on resources from healthy neighbors in the social layer. We investigate how degree heterogeneity affects the spreading dynamics. Using theoretical analysis and simulations we find that degree heterogeneity promotes disease spreading. The phase transition of the infected density is hybrid and increases smoothly from zero to a finite small value at the first invasion threshold and then suddenly jumps at the second invasion threshold. We also find a hysteresis loop in the transition of the infected density. We further investigate how an overlap in the edges between two layers affects the spreading dynamics. We find that when the amount of overlap is smaller than a critical value the phase transition is hybrid and there is a hysteresis loop, otherwise the phase transition is continuous and the hysteresis loop vanishes. In addition, the edge overlap allows an epidemic outbreak when the transmission rate is below the first invasion threshold, but suppresses any explosive transition when the transmission rate is above the first invasion threshold.
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