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Register a new userRole of bridge nodes in epidemic spreading: Different regimes and crossovers
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Power-law behaviors are common in many disciplines, especially in network science. Real-world networks, like disease spreading among people, are more likely to be interconnected communities, and show richer power-law behaviors than isolated networks. In this paper, we look at the system of two communities which are connected by bridge links between a fraction $r$ of bridge nodes, and study the effect of bridge nodes to the final state of the Susceptible-Infected-Recovered model, by mapping it to link percolation. By keeping a fixed average connectivity, but allowing different transmissibilities along internal and bridge links, we theoretically derive different power-law asymptotic behaviors of the total fraction of the recovered $R$ in the final state as $r$ goes to zero, for different combinations of internal and bridge link transmissibilities. We also find crossover points where $R$ follows different power-law behaviors with $r$ on both sides when the internal transmissibility is below but close to its critical value, for different bridge link transmissibilities. All of these power-law behaviors can be explained through different mechanisms of how finite clusters in each community are connected into the giant component of the whole system, and enable us to pick effective epidemic strategies and to better predict their impacts.
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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.
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.
Most models of epidemic spread, including many designed specifically for COVID-19, implicitly assume that social networks are undirected, i.e., that the infection is equally likely to spread in either direction whenever a contact occurs. In particular, this assumption implies that the individuals most likely to spread the disease are also the most likely to receive it from others. Here, we review results from the theory of random directed graphs which show that many important quantities, including the reproductive number and the epidemic size, depend sensitively on the joint distribution of in- and out-degrees (risk and spread), including their heterogeneity and the correlation between them. By considering joint distributions of various kinds we elucidate why some types of heterogeneity cause a deviation from the standard Kermack-McKendrick analysis of SIR models, i.e., so called mass-action models where contacts are homogeneous and random, and some do not. We also show that some structured SIR models informed by complex contact patterns among types of individuals (age or activity) are simply mixtures of Poisson processes and tend not to deviate significantly from the simplest mass-action model. Finally, we point out some possible policy implications of this directed structure, both for contact tracing strategy and for interventions designed to prevent superspreading events. In particular, directed networks have a forward and backward version of the classic friendship paradox -- forward links tend to lead to individuals with high risk, while backward links lead to individuals with high spread -- such that a combination of both forward and backward contact tracing is necessary to find superspreading events and prevent future cascades of infection.
In this work, we address a multicoupled dynamics on complex networks with tunable structural segregation. Specifically, we work on a networked epidemic spreading under a vaccination campaign with agents in favor and against the vaccine. Our results show that such coupled dynamics exhibits a myriad of phenomena such as nonequilibrium transitions accompanied by bistability. Besides we observe the emergence of an intermediate optimal segregation level where the community structure enhances negative opinions over vaccination but counterintuitively hinders - rather than favoring - the global disease spreading. Thus, our results hint vaccination campaigns should avoid policies that end up segregating excessively anti-vaccine groups so that they effectively work as echo chambers in which individuals look to confirmation without jeopardising the safety of the whole population.
In the past few decades, the frequency of pandemics has been increased due to the growth of urbanization and mobility among countries. Since a disease spreading in one country could become a pandemic with a potential worldwide humanitarian and economic impact, it is important to develop models to estimate the probability of a worldwide pandemic. In this paper, we propose a model of disease spreading in a structural modular complex network (having communities) and study how the number of bridge nodes $n$ that connect communities affects disease spread. We find that our model can be described at a global scale as an infectious transmission process between communities with global infectious and recovery time distributions that depend on the internal structure of each community and $n$. We find that near the critical point as $n$ increases, the disease reaches most of the communities, but each community has only a small fraction of recovered nodes. In addition, we obtain that in the limit $n to infty$, the probability of a pandemic increases abruptly at the critical point. This scenario could make the decision on whether to launch a pandemic alert or not more difficult. Finally, we show that link percolation theory can be used at a global scale to estimate the probability of a pandemic since the global transmissibility between communities has a weak dependence on the global recovery time.
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