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Register a new userImpact of the distribution of recovery rates on disease spreading in complex networks
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We study a general epidemic model with arbitrary recovery rate distributions. This simple deviation from the standard setup is sufficient to prove that heterogeneity in the dynamical parameters can be as important as the more studied structural heterogeneity. Our analytical solution is able to predict the shift in the critical properties induced by heterogeneous recovery rates. Additionally, we show that the critical value of infectivity tends to be smaller than the one predicted by quenched mean-field approaches in the homogeneous case and that it can be linked to the variance of the recovery rates. We then illustrate the role of dynamical--structural correlations, which allow for a complete change in the critical behavior. We show that it is possible for a power-law network topology to behave similarly to a homogeneous structure by an appropriate tuning of its recovery rates, and vice versa. Finally, we show how heterogeneity in recovery rates affects the network localization properties of the spreading process.
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We introduce a general stochastic model for the spread of rumours, and derive mean-field equations that describe the dynamics of the model on complex social networks (in particular those mediated by the Internet). We use analytical and numerical solutions of these equations to examine the threshold behavior and dynamics of the model on several models of such networks: random graphs, uncorrelated scale-free networks and scale-free networks with assortative degree correlations. We show that in both homogeneous networks and random graphs the model exhibits a critical threshold in the rumour spreading rate below which a rumour cannot propagate in the system. In the case of scale-free networks, on the other hand, this threshold becomes vanishingly small in the limit of infinite system size. We find that the initial rate at which a rumour spreads is much higher in scale-free networks than in random graphs, and that the rate at which the spreading proceeds on scale-free networks is further increased when assortative degree correlations are introduced. The impact of degree correlations on the final fraction of nodes that ever hears a rumour, however, depends on the interplay between network topology and the rumour spreading rate. Our results show that scale-free social networks are prone to the spreading of rumours, just as they are to the spreading of infections. They are relevant to the spreading dynamics of chain emails, viral advertising and large-scale information dissemination algorithms on the Internet.
Spreading processes have been largely studied in the literature, both analytically and by means of large-scale numerical simulations. These processes mainly include the propagation of diseases, rumors and information on top of a given population. In the last two decades, with the advent of modern network science, we have witnessed significant advances in this field of research. Here we review the main theoretical and numerical methods developed for the study of spreading processes on complex networked systems. Specifically, we formally define epidemic processes on single and multilayer networks and discuss in detail the main methods used to perform numerical simulations. Throughout the review, we classify spreading processes (disease and rumor models) into two classes according to the nature of time: (i) continuous-time and (ii) cellular automata approach, where the second one can be further divided into synchronous and asynchronous updating schemes. Our revision includes the heterogeneous mean-field, the quenched-mean field, and the pair quenched mean field approaches, as well as their respective simulation techniques, emphasizing similarities and differences among the different techniques. The content presented here offers a whole suite of methods to study epidemic-like processes in complex networks, both for researchers without previous experience in the subject and for experts.
Models of disease spreading are critical for predicting infection growth in a population and evaluating public health policies. However, standard models typically represent the dynamics of disease transmission between individuals using macroscopic parameters that do not accurately represent person-to-person variability. To address this issue, we present a dynamic network model that provides a straightforward way to incorporate both disease transmission dynamics at the individual scale as well as the full spatiotemporal history of infection at the population scale. We find that disease spreads through a social network as a traveling wave of infection, followed by a traveling wave of recovery, with the onset and dynamics of spreading determined by the interplay between disease transmission and recovery. We use these insights to develop a scaling theory that predicts the dynamics of infection for diverse diseases and populations. Furthermore, we show how spatial heterogeneities in susceptibility to infection can either exacerbate or quell the spread of disease, depending on its infectivity. Ultimately, our dynamic network approach provides a simple way to model disease spreading that unifies previous findings and can be generalized to diverse diseases, containment strategies, seasonal conditions, and community structures.
Spreading processes are ubiquitous in natural and artificial systems. They can be studied via a plethora of models, depending on the specific details of the phenomena under study. Disease contagion and rumor spreading are among the most important of these processes due to their practical relevance. However, despite the similarities between them, current models address both spreading dynamics separately. In this paper, we propose a general information spreading model that is based on discrete time Markov chains. The model includes all the transitions that are plausible for both a disease contagion process and rumor propagation. We show that our model not only covers the traditional spreading schemes, but that it also contains some features relevant in social dynamics, such as apathy, forgetting, and lost/recovering of interest. The model is evaluated analytically to obtain the spreading thresholds and the early time dynamical behavior for the contact and reactive processes in several scenarios. Comparison with Monte Carlo simulations shows that the Markov chain formalism is highly accurate while it excels in computational efficiency. We round off our work by showing how the proposed framework can be applied to the study of spreading processes occurring on social networks.
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.
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