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Suppressing disease spreading by using information diffusion on multiplex networks.

ABSTRACT: Although there is always an interplay between the dynamics of information diffusion and disease spreading, the empirical research on the systemic coevolution mechanisms connecting these two spreading dynamics is still lacking. Here we investigate the coevolution mechanisms and dynamics between information and disease spreading by utilizing real data and a proposed spreading model on multiplex network. Our empirical analysis finds asymmetrical interactions between the information and disease spreading dynamics. Our results obtained from both the theoretical framework and extensive stochastic numerical simulations suggest that an information outbreak can be triggered in a communication network by its own spreading dynamics or by a disease outbreak on a contact network, but that the disease threshold is not affected by information spreading. Our key finding is that there is an optimal information transmission rate that markedly suppresses the disease spreading. We find that the time evolution of the dynamics in the proposed model qualitatively agrees with the real-world spreading processes at the optimal information transmission rate.

SUBMITTER: Wang W

PROVIDER: S-EPMC4933956 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Suppressing disease spreading by using information diffusion on multiplex networks.

Wang Wei W Liu Quan-Hui QH Cai Shi-Min SM Tang Ming M Braunstein Lidia A LA Stanley H Eugene HE

Scientific reports 20160706

Although there is always an interplay between the dynamics of information diffusion and disease spreading, the empirical research on the systemic coevolution mechanisms connecting these two spreading dynamics is still lacking. Here we investigate the coevolution mechanisms and dynamics between information and disease spreading by utilizing real data and a proposed spreading model on multiplex network. Our empirical analysis finds asymmetrical interactions between the information and disease spre ...[more]

PMID: 27380881

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Project description:We propose a theoretical framework for the study of spreading processes in structured metapopulations, with heterogeneous agents, subjected to different recurrent mobility patterns. We propose to represent the heterogeneity in the composition of the metapopulations as layers in a multiplex network, where nodes would correspond to geographical areas and layers account for the mobility patterns of agents of the same class. We analyze classical epidemic models within this framework and obtain an excellent agreement with extensive Monte Carlo simulations. This agreement allows us to derive analytical expressions of the epidemic threshold and to face the challenge of characterizing a real multiplex metapopulation, the city of Medellín in Colombia, where different recurrent mobility patterns are observed depending on the socioeconomic class of the agents. Our framework allows us to unveil the geographical location of those patches that trigger the epidemic state at the critical point. A careful exploration reveals that social mixing between classes and mobility crucially determines these critical patches and, more importantly, it can produce abrupt changes of the critical properties of the epidemic onset. Summary The spread of disease is strongly driven by how humans move and segregate across cities, regions, and countries. Understanding how epidemics arise from the interplay of these behaviors is crucial for implementing efficient containment and prevention policies. In this work, we propose a theoretical framework for the spread of pathogens that incorporates the real patterns of mobility, demographics, and human diversity observed in urban environments. Our framework represents various populations in a community as layers in a multiplex network, where nodes correspond to geographical areas and layers account for movement patterns. With this framework, we analyze a real urban system, the city of Medellin in Colombia, considering the interplay between six socioeconomic classes displaying disparate demographic segregation and mobility habits. Our framework can identify those neighborhoods and classes that trigger epidemic outbreaks. Remarkably, we observe that small changes to both mobility and social mixing among these subpopulations can trigger abrupt changes. As a consequence, containment strategies targeting a certain neighborhood can quickly change from efficient to useless. Finally, we provide a physical interpretation of the abrupt changes of those patches driving the unfolding of epidemics based on the effective number of contacts of agents. Our framework provides a reliable, time-saving platform for analyzing the spread of pathogens among various populations, allowing researchers to identify areas critical to the unfolding of diseases. With further improvements, our formalism could be extended to accommodate more sophisticated commuting patterns and epidemic models.

Project description:Progress has been made in understanding how temporal network features affect the percentage of nodes reached by an information diffusion process. In this work, we explore further: which node pairs are likely to contribute to the actual diffusion of information, i.e., appear in a diffusion trajectory? How is this likelihood related to the local temporal connection features of the node pair? Such deep understanding of the role of node pairs is crucial to tackle challenging optimization problems such as which kind of node pairs or temporal contacts should be stimulated in order to maximize the prevalence of information spreading. We start by using Susceptible-Infected (SI) model, in which an infected (information possessing) node could spread the information to a susceptible node with a given infection probability ? whenever a contact happens between the two nodes, as the information diffusion process. We consider a large number of real-world temporal networks. First, we propose the construction of an information diffusion backbone GB(?) for a SI spreading process with an infection probability ? on a temporal network. The backbone is a weighted network where the weight of each node pair indicates how likely the node pair appears in a diffusion trajectory starting from an arbitrary node. Second, we investigate the relation between the backbones with different infection probabilities on a temporal network. We find that the backbone topology obtained for low and high infection probabilities approach the backbone GB(????0) and GB(??=?1), respectively. The backbone GB(????0) equals the integrated weighted network, where the weight of a node pair counts the total number of contacts in between. Finally, we explore node pairs with what local connection features tend to appear in GB(??=?1), thus actually contribute to the global information diffusion. We discover that a local connection feature among many other features we proposed, could well identify the (high-weight) links in GB(??=?1). This local feature encodes the time that each contact occurs, pointing out the importance of temporal features in determining the role of node pairs in a dynamic process.

Dataset Information

Suppressing disease spreading by using information diffusion on multiplex networks.

Publications

Suppressing disease spreading by using information diffusion on multiplex networks.

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