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      On the Use of Human Mobility Proxies for Modeling Epidemics

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          Abstract

          Human mobility is a key component of large-scale spatial-transmission models of infectious diseases. Correctly modeling and quantifying human mobility is critical for improving epidemic control, but may be hindered by data incompleteness or unavailability. Here we explore the opportunity of using proxies for individual mobility to describe commuting flows and predict the diffusion of an influenza-like-illness epidemic. We consider three European countries and the corresponding commuting networks at different resolution scales, obtained from (i) official census surveys, (ii) proxy mobility data extracted from mobile phone call records, and (iii) the radiation model calibrated with census data. Metapopulation models defined on these countries and integrating the different mobility layers are compared in terms of epidemic observables. We show that commuting networks from mobile phone data capture the empirical commuting patterns well, accounting for more than 87% of the total fluxes. The distributions of commuting fluxes per link from mobile phones and census sources are similar and highly correlated, however a systematic overestimation of commuting traffic in the mobile phone data is observed. This leads to epidemics that spread faster than on census commuting networks, once the mobile phone commuting network is considered in the epidemic model, however preserving to a high degree the order of infection of newly affected locations. Proxies' calibration affects the arrival times' agreement across different models, and the observed topological and traffic discrepancies among mobility sources alter the resulting epidemic invasion patterns. Results also suggest that proxies perform differently in approximating commuting patterns for disease spread at different resolution scales, with the radiation model showing higher accuracy than mobile phone data when the seed is central in the network, the opposite being observed for peripheral locations. Proxies should therefore be chosen in light of the desired accuracy for the epidemic situation under study.

          Author Summary

          The spatial dissemination of a directly transmitted infectious disease in a population is driven by population movements from one region to another allowing mixing and importation. Public health policy and planning may thus be more accurate if reliable descriptions of population movements can be considered in the epidemic evaluations. Next to census data, generally available in developed countries, alternative solutions can be found to describe population movements where official data is missing. These include mobility models, such as the radiation model, and the analysis of mobile phone activity records providing individual geo-temporal information. Here we explore to what extent mobility proxies, such as mobile phone data or mobility models, can effectively be used in epidemic models for influenza-like-illnesses and how they compare to official census data. By focusing on three European countries, we find that phone data matches the commuting patterns reported by census well but tends to overestimate the number of commuters, leading to a faster diffusion of simulated epidemics. The order of infection of newly infected locations is however well preserved, whereas the pattern of epidemic invasion is captured with higher accuracy by the radiation model for centrally seeded epidemics and by phone proxy for peripherally seeded epidemics.

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          Most cited references30

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          Human Infection with a Novel Avian-Origin Influenza A (H7N9) Virus

          New England Journal of Medicine, 368(20), 1888-1897
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            Understanding individual human mobility patterns

            Despite their importance for urban planning, traffic forecasting, and the spread of biological and mobile viruses, our understanding of the basic laws governing human motion remains limited thanks to the lack of tools to monitor the time resolved location of individuals. Here we study the trajectory of 100,000 anonymized mobile phone users whose position is tracked for a six month period. We find that in contrast with the random trajectories predicted by the prevailing Levy flight and random walk models, human trajectories show a high degree of temporal and spatial regularity, each individual being characterized by a time independent characteristic length scale and a significant probability to return to a few highly frequented locations. After correcting for differences in travel distances and the inherent anisotropy of each trajectory, the individual travel patterns collapse into a single spatial probability distribution, indicating that despite the diversity of their travel history, humans follow simple reproducible patterns. This inherent similarity in travel patterns could impact all phenomena driven by human mobility, from epidemic prevention to emergency response, urban planning and agent based modeling.
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              Modelling the influence of human behaviour on the spread of infectious diseases: a review.

              Human behaviour plays an important role in the spread of infectious diseases, and understanding the influence of behaviour on the spread of diseases can be key to improving control efforts. While behavioural responses to the spread of a disease have often been reported anecdotally, there has been relatively little systematic investigation into how behavioural changes can affect disease dynamics. Mathematical models for the spread of infectious diseases are an important tool for investigating and quantifying such effects, not least because the spread of a disease among humans is not amenable to direct experimental study. Here, we review recent efforts to incorporate human behaviour into disease models, and propose that such models can be broadly classified according to the type and source of information which individuals are assumed to base their behaviour on, and according to the assumed effects of such behaviour. We highlight recent advances as well as gaps in our understanding of the interplay between infectious disease dynamics and human behaviour, and suggest what kind of data taking efforts would be helpful in filling these gaps.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS Comput Biol
                PLoS Comput. Biol
                plos
                ploscomp
                PLoS Computational Biology
                Public Library of Science (San Francisco, USA )
                1553-734X
                1553-7358
                July 2014
                10 July 2014
                : 10
                : 7
                : e1003716
                Affiliations
                [1 ]Computational Epidemiology Laboratory, Institute for Scientific Interchange (ISI), Torino, Italy
                [2 ]Department of Veterinary Science, University of Turin, Torino, Italy
                [3 ]ICTEAM Institute, Université Catholique de Louvain, Louvain-la-Neuve, Belgium
                [4 ]CNRS, UMR5558, F-69622 Villeurbanne, France
                [5 ]Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America
                [6 ]Sociology and Economics of Networks and Services Department, Orange Labs, Issy-les-Moulineaux, France
                [7 ]Engineering Systems Division, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America
                [8 ]INSERM, U707, Paris, France
                [9 ]UPMC Université Paris 06, Faculté de Médecine Pierre et Marie Curie, UMR S 707, Paris, France
                [10 ]Institute for Scientific Interchange (ISI), Torino, Italy
                Pennsylvania State University, United States of America
                Author notes

                The authors have declared that no competing interests exist.

                Conceived and designed the experiments: VC. Performed the experiments: MT PB. Analyzed the data: MT PB AD GKKK CMS. Contributed reagents/materials/analysis tools: MT PB AD GKKK CMS VB ZS MCG VC. Wrote the paper: MT PB AD GKKK CMS VB ZS MCG VC. Drafted the manuscript: MT PB VC.

                Article
                PCOMPBIOL-D-13-01711
                10.1371/journal.pcbi.1003716
                4091706
                25010676
                7f475bb7-e6ae-4ca7-86c3-ee18a7ff6580
                Copyright @ 2014

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 30 September 2013
                : 22 May 2014
                Page count
                Pages: 15
                Funding
                This work has been partially funded by the ERC Ideas contract n.ERC-2007-Stg204863 (EpiFor) to MT, PB, VC; ANR contract no. ANR-12-MONU-0018 (HARMSFLU) to VC. AD is a research fellow with the Fonds National de la Recherche Scientifique (FRS-FNRS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology and Life Sciences
                Computational Biology
                Population Modeling
                Infectious Disease Modeling

                Quantitative & Systems biology
                Quantitative & Systems biology

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