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Register a new userControlling Contagion Processes in Time-Varying Networks
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The vast majority of strategies aimed at controlling contagion processes on networks considers the connectivity pattern of the system as either quenched or annealed. However, in the real world many networks are highly dynamical and evolve in time concurrently to the contagion process. Here, we derive an analytical framework for the study of control strategies specifically devised for time-varying networks. We consider the removal/immunization of individual nodes according the their activity in the network and develop a block variable mean-field approach that allows the derivation of the equations describing the evolution of the contagion process concurrently to the network dynamic. We derive the critical immunization threshold and assess the effectiveness of the control strategies. Finally, we validate the theoretical picture by simulating numerically the information spreading process and control strategies in both synthetic networks and a large-scale, real-world mobile telephone call dataset
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The metapopulation framework is adopted in a wide array of disciplines to describe systems of well separated yet connected subpopulations. The subgroups or patches are often represented as nodes in a network whose links represent the migration routes among them. The connections have been so far mostly considered as static, but in general evolve in time. Here we address this case by investigating simple contagion processes on time-varying metapopulation networks. We focus on the SIR process and determine analytically the mobility threshold for the onset of an epidemic spreading in the framework of activity-driven network models. We find profound differences from the case of static networks. The threshold is entirely described by the dynamical parameters defining the average number of instantaneously migrating individuals and does not depend on the properties of the static network representation. Remarkably, the diffusion and contagion processes are slower in time-varying graphs than in their aggregated static counterparts, the mobility threshold being even two orders of magnitude larger in the first case. The presented results confirm the importance of considering the time-varying nature of complex networks.
This paper mainly discusses the diffusion on complex networks with time-varying couplings. We propose a model to describe the adaptive diffusion process of local topological and dynamical information, and find that the Barabasi-Albert scale-free network (BA network) is beneficial to the diffusion and leads nodes to arrive at a larger state value than other networks do. The ability of diffusion for a node is related to its own degree. Specifically, nodes with smaller degrees are more likely to change their states and reach larger values, while those with larger degrees tend to stick to their original states. We introduce state entropy to analyze the thermodynamic mechanism of the diffusion process, and interestingly find that this kind of diffusion process is a minimization process of state entropy. We use the inequality constrained optimization method to reveal the restriction function of the minimization and find that it has the same form as the Gibbs free energy. The thermodynamical concept allows us to understand dynamical processes on complex networks from a brand-new perspective. The result provides a convenient means of optimizing relevant dynamical processes on practical circuits as well as related complex systems.
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
Complex networks represent the natural backbone to study epidemic processes in populations of interacting individuals. Such a modeling framework, however, is naturally limited to pairwise interactions, making it less suitable to properly describe social contagion, where individuals acquire new norms or ideas after simultaneous exposure to multiple sources of infections. Simplicial contagion has been proposed as an alternative framework where simplices are used to encode group interactions of any order. The presence of higher-order interactions leads to explosive epidemic transitions and bistability which cannot be obtained when only dyadic ties are considered. In particular, critical mass effects can emerge even for infectivity values below the standard pairwise epidemic threshold, where the size of the initial seed of infectious nodes determines whether the system would eventually fall in the endemic or the healthy state. Here we extend simplicial contagion to time-varying networks, where pairwise and higher-order simplices can be created or destroyed over time. By following a microscopic Markov chain approach, we find that the same seed of infectious nodes might or might not lead to an endemic stationary state, depending on the temporal properties of the underlying network structure, and show that persistent temporal interactions anticipate the onset of the endemic state in finite-size systems. We characterize this behavior on higher-order networks with a prescribed temporal correlation between consecutive interactions and on heterogeneous simplicial complexes, showing that temporality again limits the effect of higher-order spreading, but in a less pronounced way than for homogeneous structures. Our work suggests the importance of incorporating temporality, a realistic feature of many real-world systems, into the investigation of dynamical processes beyond pairwise interactions.
Stochastic simulations are one of the cornerstones of the analysis of dynamical processes on complex networks, and are often the only accessible way to explore their behavior. The development of fast algorithms is paramount to allow large-scale simulations. The Gillespie algorithm can be used for fast simulation of stochastic processes, and variants of it have been applied to simulate dynamical processes on static networks. However, its adaptation to temporal networks remains non-trivial. We here present a temporal Gillespie algorithm that solves this problem. Our method is applicable to general Poisson (constant-rate) processes on temporal networks, stochastically exact, and up to multiple orders of magnitude faster than traditional simulation schemes based on rejection sampling. We also show how it can be extended to simulate non-Markovian processes. The algorithm is easily applicable in practice, and as an illustration we detail how to simulate both Poissonian and non-Markovian models of epidemic spreading. Namely, we provide pseudocode and its implementation in C++ for simulating the paradigmatic Susceptible-Infected-Susceptible and Susceptible-Infected-Recovered models and a Susceptible-Infected-Recovered model with non-constant recovery rates. For empirical networks, the temporal Gillespie algorithm is here typically from 10 to 100 times faster than rejection sampling.
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