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Register a new userTemporal percolation of the susceptible network in an epidemic spreading
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In this work, we study the evolution of the susceptible individuals during the spread of an epidemic modeled by the susceptible-infected-recovered (SIR) process spreading on the top of complex networks. Using an edge-based compartmental approach and percolation tools, we find that a time-dependent quantity $Phi_S(t)$, namely, the probability that a given neighbor of a node is susceptible at time $t$, is the control parameter of a node void percolation process involving those nodes on the network not-reached by the disease. We show that there exists a critical time $t_c$ above which the giant susceptible component is destroyed. As a consequence, in order to preserve a macroscopic connected fraction of the network composed by healthy individuals which guarantee its functionality, any mitigation strategy should be implemented before this critical time $t_c$. Our theoretical results are confirmed by extensive simulations of the SIR process.
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In the last decades, many authors have used the susceptible-infected-recovered model to study the impact of the disease spreading on the evolution of the infected individuals. However, few authors focused on the temporal unfolding of the susceptible individuals. In this paper, we study the dynamic of the susceptible-infected-recovered model in an adaptive network that mimics the transitory deactivation of permanent social contacts, such as friendship and work-ship ties. Using an edge-based compartmental model and percolation theory, we obtain the evolution equations for the fraction susceptible individuals in the susceptible biggest component. In particular, we focus on how the individuals behavior impacts on the dilution of the susceptible network. We show that, as a consequence, the spreading of the disease slows down, protecting the biggest susceptible cluster by increasing the critical time at which the giant susceptible component is destroyed. Our theoretical results are fully supported by extensive simulations.
Understanding spreading dynamics will benefit society as a whole in better preventing and controlling diseases, as well as facilitating the socially responsible information while depressing destructive rumors. In network-based spreading dynamics, edges with different weights may play far different roles: a friend from afar usually brings novel stories, and an intimate relationship is highly risky for a flu epidemic. In this article, we propose a weighted susceptible-infected-susceptible model on complex networks, where the weight of an edge is defined by the topological proximity of the two associated nodes. Each infected individual is allowed to select limited number of neighbors to contact, and a tunable parameter is introduced to control the preference to contact through high-weight or low-weight edges. Experimental results on six real networks show that the epidemic prevalence can be largely promoted when strong ties are favored in the spreading process. By comparing with two statistical null models respectively with randomized topology and randomly redistributed weights, we show that the distribution pattern of weights, rather than the topology, mainly contributes to the experimental observations. Further analysis suggests that the weight-weight correlation strongly affects the results: high-weight edges are more significant in keeping high epidemic prevalence when the weight-weight correlation is present.
Time-varying network topologies can deeply influence dynamical processes mediated by them. Memory effects in the pattern of interactions among individuals are also known to affect how diffusive and spreading phenomena take place. In this paper we analyze the combined effect of these two ingredients on epidemic dynamics on networks. We study the susceptible-infected-susceptible (SIS) and the susceptible-infected-removed (SIR) models on the recently introduced activity-driven networks with memory. By means of an activity-based mean-field approach we derive, in the long time limit, analytical predictions for the epidemic threshold as a function of the parameters describing the distribution of activities and the strength of the memory effects. Our results show that memory reduces the threshold, which is the same for SIS and SIR dynamics, therefore favouring epidemic spreading. The theoretical approach perfectly agrees with numerical simulations in the long time asymptotic regime. Strong aging effects are present in the preasymptotic regime and the epidemic threshold is deeply affected by the starting time of the epidemics. We discuss in detail the origin of the model-dependent preasymptotic corrections, whose understanding could potentially allow for epidemic control on correlated temporal networks.
Dynamic networks exhibit temporal patterns that vary across different time scales, all of which can potentially affect processes that take place on the network. However, most data-driven approaches used to model time-varying networks attempt to capture only a single characteristic time scale in isolation --- typically associated with the short-time memory of a Markov chain or with long-time abrupt changes caused by external or systemic events. Here we propose a unified approach to model both aspects simultaneously, detecting short and long-time behaviors of temporal networks. We do so by developing an arbitrary-order mixed Markov model with change points, and using a nonparametric Bayesian formulation that allows the Markov order and the position of change points to be determined from data without overfitting. In addition, we evaluate the quality of the multiscale model in its capacity to reproduce the spreading of epidemics on the temporal network, and we show that describing multiple time scales simultaneously has a synergistic effect, where statistically significant features are uncovered that otherwise would remain hidden by treating each time scale independently.
This study is concerned with the dynamical behaviors of epidemic spreading over a two-layered interconnected network. Three models in different levels are proposed to describe cooperative spreading processes over the interconnected network, wherein the disease in one network can spread to the other. Theoretical analysis is provided for each model to reveal that the global epidemic threshold in the interconnected network is not larger than the epidemic thresholds for the two isolated layered networks. In particular, in an interconnected homogenous network, detailed theoretical analysis is presented, which allows quick and accurate calculations of the global epidemic threshold. Moreover, in an interconnected heterogeneous network with inter-layer correlation between node degrees, it is found that the inter-layer correlation coefficient has little impact on the epidemic threshold, but has significant impact on the total prevalence. Simulations further verify the analytical results, showing that cooperative epidemic processes promote the spreading of diseases.
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