No Arabic abstract
Improved mobility not only contributes to more intensive human activities but also facilitates the spread of communicable disease, thus constituting a major threat to billions of urban commuters. In this study, we present a multi-city investigation of communicable diseases percolating among metro travelers. We use smart card data from three megacities in China to construct individual-level contact networks, based on which the spread of disease is modeled and studied. We observe that, though differing in urban forms, network layouts, and mobility patterns, the metro systems of the three cities share similar contact network structures. This motivates us to develop a universal generation model that captures the distributions of the number of contacts as well as the contact duration among individual travelers. This model explains how the structural properties of the metro contact network are associated with the risk level of communicable diseases. Our results highlight the vulnerability of urban mass transit systems during disease outbreaks and suggest important planning and operation strategies for mitigating the risk of communicable diseases.
Background: Zipfs law and Heaps law are two representatives of the scaling concepts, which play a significant role in the study of complexity science. The coexistence of the Zipfs law and the Heaps law motivates different understandings on the dependence between these two scalings, which is still hardly been clarified. Methodology/Principal Findings: In this article, we observe an evolution process of the scalings: the Zipfs law and the Heaps law are naturally shaped to coexist at the initial time, while the crossover comes with the emergence of their inconsistency at the larger time before reaching a stable state, where the Heaps law still exists with the disappearance of strict Zipfs law. Such findings are illustrated with a scenario of large-scale spatial epidemic spreading, and the empirical results of pandemic disease support a universal analysis of the relation between the two laws regardless of the biological details of disease. Employing the United States(U.S.) domestic air transportation and demographic data to construct a metapopulation model for simulating the pandemic spread at the U.S. country level, we uncover that the broad heterogeneity of the infrastructure plays a key role in the evolution of scaling emergence. Conclusions/Significance: The analyses of large-scale spatial epidemic spreading help understand the temporal evolution of scalings, indicating the coexistence of the Zipfs law and the Heaps law depends on the collective dynamics of epidemic processes, and the heterogeneity of epidemic spread indicates the significance of performing targeted containment strategies at the early time of a pandemic disease.
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.
The spread of an infection on a real-world social network is determined by the interplay of two processes: the dynamics of the network, whose structure changes over time according to the encounters between individuals, and the dynamics on the network, whose nodes can infect each other after an encounter. Physical encounter is the most common vehicle for the spread of infectious diseases, but detailed information about encounters is often unavailable because expensive, unpractical to collect or privacy sensitive. We asks whether the friendship ties between the individuals in a social network successfully predict who is at risk. Using a dataset from a popular online review service, we build a time-varying network that is a proxy of physical encounter between users and a static network based on reported friendship. Through computer simulations, we compare infection processes on the resulting networks and show that, whereas distance on the friendship network is correlated to epidemic risk, friendship provides a poor identification of the individuals at risk if the infection is driven by physical encounter. Such limit is not due to the randomness of the infection, but to the structural differences of the two networks. In contrast to the macroscopic similarity between processes spreading on different networks, the differences in local connectivity determined by the two definitions of edges result in striking differences between the dynamics at a microscopic level. Despite the limits highlighted, we show that periodical and relatively infrequent monitoring of the real infection on the encounter network allows to correct the predicted infection on the friendship network and to achieve satisfactory prediction accuracy. In addition, the friendship network contains valuable information to effectively contain epidemic outbreaks when a limited budget is available for immunization.
In spite of the extensive previous efforts on traffic dynamics and epidemic spreading in complex networks, the problem of traffic-driven epidemic spreading on {em correlated} networks has not been addressed. Interestingly, we find that the epidemic threshold, a fundamental quantity underlying the spreading dynamics, exhibits a non-monotonic behavior in that it can be minimized for some critical value of the assortativity coefficient, a parameter characterizing the network correlation. To understand this phenomenon, we use the degree-based mean-field theory to calculate the traffic-driven epidemic threshold for correlated networks. The theory predicts that the threshold is inversely proportional to the packet-generation rate and the largest eigenvalue of the betweenness matrix. We obtain consistency between theory and numerics. Our results may provide insights into the important problem of controlling/harnessing real-world epidemic spreading dynamics driven by traffic flows.
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