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Register a new userUnification of theoretical approaches for epidemic spreading on complex networks
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Models of epidemic spreading on complex networks have attracted great attention among researchers in physics, mathematics, and epidemiology due to their success in predicting and controlling scenarios of epidemic spreading in real-world scenarios. To understand the interplay between epidemic spreading and the topology of a contact network, several outstanding theoretical approaches have been developed. An accurate theoretical approach describing the spreading dynamics must take both the network topology and dynamical correlations into consideration at the expense of increasing the complexity of the equations. In this short survey we unify the most widely used theoretical approaches for epidemic spreading on complex networks in terms of increasing complexity, including the mean-field, the heterogeneous mean-field, the quench mean-field, dynamical message-passing, link percolation, and pairwise approximation. We build connections among these approaches to provide new insights into developing an accurate theoretical approach to spreading dynamics on complex networks.
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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
A model for epidemic spreading on rewiring networks is introduced and analyzed for the case of scale free steady state networks. It is found that contrary to what one would have naively expected, the rewiring process typically tends to suppress epidemic spreading. In particular it is found that as in static networks, rewiring networks with degree distribution exponent $gamma >3$ exhibit a threshold in the infection rate below which epidemics die out in the steady state. However the threshold is higher in the rewiring case. For $2<gamma leq 3$ no such threshold exists, but for small infection rate the steady state density of infected nodes (prevalence) is smaller for rewiring networks.
We study SIS epidemic spreading processes unfolding on a recent generalisation of the activity-driven modelling framework. In this model of time-varying networks each node is described by two variables: activity and attractiveness. The first, describes the propensity to form connections. The second, defines the propensity to attract them. We derive analytically the epidemic threshold considering the timescale driving the evolution of contacts and the contagion as comparable. The solutions are general and hold for any joint distribution of activity and attractiveness. The theoretical picture is confirmed via large-scale numerical simulations performed considering heterogeneous distributions and different correlations between the two variables. We find that heterogeneous distributions of attractiveness alter the contagion process. In particular, in case of uncorrelated and positive correlations between the two variables, heterogeneous attractiveness facilitates the spreading. On the contrary, negative correlations between activity and attractiveness hamper the spreading. The results presented contribute to the understanding of the dynamical properties of time-varying networks and their effects on contagion phenomena unfolding on their fabric.
Albeit epidemic models have evolved into powerful predictive tools for the spread of diseases and opinions, most assume memoryless agents and independent transmission channels. We develop an infection mechanism that is endowed with memory of past exposures and simultaneously incorporates the joint effect of multiple infectious sources. Analytic equations and simulations of the susceptible-infected-susceptible model in unstructured substrates reveal the emergence of an additional phase that separates the usual healthy and endemic ones. This intermediate phase shows fundamentally distinct characteristics, and the system exhibits either excitability or an exotic variant of bistability. Moreover, the transition to endemicity presents hybrid aspects. These features are the product of an intricate balance between two memory modes and indicate that non-Markovian effects significantly alter the properties of spreading processes.
We investigate the effect of degree correlation on a susceptible-infected-susceptible (SIS) model with a nonlinear cooperative effect (synergy) in infectious transmissions. In a mean-field treatment of the synergistic SIS model on a bimodal network with tunable degree correlation, we identify a discontinuous transition that is independent of the degree correlation strength unless the synergy is absent or extremely weak. Regardless of synergy (absent or present), a positive and negative degree correlation in the model reduces and raises the epidemic threshold, respectively. For networks with a strongly positive degree correlation, the mean-field treatment predicts the emergence of two discontinuous jumps in the steady-state infected density. To test the mean-field treatment, we provide approximate master equations of the present model, which accurately describe the synergistic SIS dynamics. We quantitatively confirm all qualitative predictions of the mean-field treatment in numerical evaluations of the approximate master equations.
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