51,882 research outputs found

    Probing empirical contact networks by simulation of spreading dynamics

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    Disease, opinions, ideas, gossip, etc. all spread on social networks. How these networks are connected (the network structure) influences the dynamics of the spreading processes. By investigating these relationships one gains understanding both of the spreading itself and the structure and function of the contact network. In this chapter, we will summarize the recent literature using simulation of spreading processes on top of empirical contact data. We will mostly focus on disease simulations on temporal proximity networks -- networks recording who is close to whom, at what time -- but also cover other types of networks and spreading processes. We analyze 29 empirical networks to illustrate the methods

    Epidemic spreading on preferred degree adaptive networks

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    We study the standard SIS model of epidemic spreading on networks where individuals have a fluctuating number of connections around a preferred degree κ\kappa . Using very simple rules for forming such preferred degree networks, we find some unusual statistical properties not found in familiar Erd\H{o}s-R\'{e}nyi or scale free networks. By letting κ\kappa depend on the fraction of infected individuals, we model the behavioral changes in response to how the extent of the epidemic is perceived. In our models, the behavioral adaptations can be either `blind' or `selective' -- depending on whether a node adapts by cutting or adding links to randomly chosen partners or selectively, based on the state of the partner. For a frozen preferred network, we find that the infection threshold follows the heterogeneous mean field result λc/μ=/\lambda_{c}/\mu =/ and the phase diagram matches the predictions of the annealed adjacency matrix (AAM) approach. With `blind' adaptations, although the epidemic threshold remains unchanged, the infection level is substantially affected, depending on the details of the adaptation. The `selective' adaptive SIS models are most interesting. Both the threshold and the level of infection changes, controlled not only by how the adaptations are implemented but also how often the nodes cut/add links (compared to the time scales of the epidemic spreading). A simple mean field theory is presented for the selective adaptations which capture the qualitative and some of the quantitative features of the infection phase diagram.Comment: 21 pages, 7 figure

    Mathematical Modeling of Trending Topics on Twitter

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    Created in 2006, Twitter is an online social networking service in which users share and read 140-character messages called Tweets. The site has approximately 288 million monthly active users who produce about 500 million Tweets per day. This study applies dynamical and statistical modeling strategies to quantify the spread of information on Twitter. Parameter estimates for the rates of infection and recovery are obtained using Bayesian Markov Chain Monte Carlo (MCMC) methods. The methodological strategy employed is an extension of techniques traditionally used in an epidemiological and biomedical context (particularly in the spread of infectious disease). This study, which addresses information spread, presents case studies pertaining to the prevalence of several “trending” topics on Twitter over time. The study introduces a framework to compare information dynamics on Twitter based on the topical area as well as a framework for the prediction of topic prevalence. Additionally, methodological and results-based comparisons are drawn between the spread of information and the spread of infectious disease

    Network Inoculation: Heteroclinics and phase transitions in an epidemic model

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    In epidemiological modelling, dynamics on networks, and in particular adaptive and heterogeneous networks have recently received much interest. Here we present a detailed analysis of a previously proposed model that combines heterogeneity in the individuals with adaptive rewiring of the network structure in response to a disease. We show that in this model qualitative changes in the dynamics occur in two phase transitions. In a macroscopic description one of these corresponds to a local bifurcation whereas the other one corresponds to a non-local heteroclinic bifurcation. This model thus provides a rare example of a system where a phase transition is caused by a non-local bifurcation, while both micro- and macro-level dynamics are accessible to mathematical analysis. The bifurcation points mark the onset of a behaviour that we call network inoculation. In the respective parameter region exposure of the system to a pathogen will lead to an outbreak that collapses, but leaves the network in a configuration where the disease cannot reinvade, despite every agent returning to the susceptible class. We argue that this behaviour and the associated phase transitions can be expected to occur in a wide class of models of sufficient complexity.Comment: 26 pages, 11 figure

    Causal Inference in Disease Spread across a Heterogeneous Social System

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    Diffusion processes are governed by external triggers and internal dynamics in complex systems. Timely and cost-effective control of infectious disease spread critically relies on uncovering the underlying diffusion mechanisms, which is challenging due to invisible causality between events and their time-evolving intensity. We infer causal relationships between infections and quantify the reflexivity of a meta-population, the level of feedback on event occurrences by its internal dynamics (likelihood of a regional outbreak triggered by previous cases). These are enabled by our new proposed model, the Latent Influence Point Process (LIPP) which models disease spread by incorporating macro-level internal dynamics of meta-populations based on human mobility. We analyse 15-year dengue cases in Queensland, Australia. From our causal inference, outbreaks are more likely driven by statewide global diffusion over time, leading to complex behavior of disease spread. In terms of reflexivity, precursory growth and symmetric decline in populous regions is attributed to slow but persistent feedback on preceding outbreaks via inter-group dynamics, while abrupt growth but sharp decline in peripheral areas is led by rapid but inconstant feedback via intra-group dynamics. Our proposed model reveals probabilistic causal relationships between discrete events based on intra- and inter-group dynamics and also covers direct and indirect diffusion processes (contact-based and vector-borne disease transmissions).Comment: arXiv admin note: substantial text overlap with arXiv:1711.0635
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