513 research outputs found

    Model-based comprehensive analysis of school closure policies for mitigating influenza epidemics and pandemics

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    School closure policies are among the non-pharmaceutical measures taken into consideration to mitigate influenza epidemics and pandemics spread. However, a systematic review of the effectiveness of alternative closure policies has yet to emerge. Here we perform a model-based analysis of four types of school closure, ranging from the nationwide closure of all schools at the same time to reactive gradual closure, starting from class-by-class, then grades and finally the whole school. We consider policies based on triggers that are feasible to monitor, such as school absenteeism and national ILI surveillance system. We found that, under specific constraints on the average number of weeks lost per student, reactive school-by-school, gradual, and county-wide closure give comparable outcomes in terms of optimal infection attack rate reduction, peak incidence reduction or peak delay. Optimal implementations generally require short closures of one week each; this duration is long enough to break the transmission chain without leading to unnecessarily long periods of class interruption. Moreover, we found that gradual and county closures may be slightly more easily applicable in practice as they are less sensitive to the value of the excess absenteeism threshold triggering the start of the intervention. These findings suggest that policy makers could consider school closure policies more diffusely as response strategy to influenza epidemics and pandemics, and the fact that some countries already have some experience of gradual or regional closures for seasonal influenza outbreaks demonstrates that logistic and feasibility challenges of school closure strategies can be to some extent overcome

    Social contact structures and time use patterns in the Manicaland Province of Zimbabwe.

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    BACKGROUND: Patterns of person-to-person contacts relevant for infectious diseases transmission are still poorly quantified in Sub-Saharan Africa (SSA), where socio-demographic structures and behavioral attitudes are expected to be different from those of more developed countries. METHODS AND FINDINGS: We conducted a diary-based survey on daily contacts and time-use of individuals of different ages in one rural and one peri-urban site of Manicaland, Zimbabwe. A total of 2,490 diaries were collected and used to derive age-structured contact matrices, to analyze time spent by individuals in different settings, and to identify the key determinants of individuals' mixing patterns. Overall 10.8 contacts per person/day were reported, with a significant difference between the peri-urban and the rural site (11.6 versus 10.2). A strong age-assortativeness characterized contacts of school-aged children, whereas the high proportion of extended families and the young population age-structure led to a significant intergenerational mixing at older ages. Individuals spent on average 67% of daytime at home, 2% at work, and 9% at school. Active participation in school and work resulted the key drivers of the number of contacts and, similarly, household size, class size, and time spent at work influenced the number of home, school, and work contacts, respectively. We found that the heterogeneous nature of home contacts is critical for an epidemic transmission chain. In particular, our results suggest that, during the initial phase of an epidemic, about 50% of infections are expected to occur among individuals younger than 12 years and less than 20% among individuals older than 35 years. CONCLUSIONS: With the current work, we have gathered data and information on the ways through which individuals in SSA interact, and on the factors that mostly facilitate this interaction. Monitoring these processes is critical to realistically predict the effects of interventions on infectious diseases dynamics

    Simulation of an SEIR infectious disease model on the dynamic contact network of conference attendees

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    The spread of infectious diseases crucially depends on the pattern of contacts among individuals. Knowledge of these patterns is thus essential to inform models and computational efforts. Few empirical studies are however available that provide estimates of the number and duration of contacts among social groups. Moreover, their space and time resolution are limited, so that data is not explicit at the person-to-person level, and the dynamical aspect of the contacts is disregarded. Here, we want to assess the role of data-driven dynamic contact patterns among individuals, and in particular of their temporal aspects, in shaping the spread of a simulated epidemic in the population. We consider high resolution data of face-to-face interactions between the attendees of a conference, obtained from the deployment of an infrastructure based on Radio Frequency Identification (RFID) devices that assess mutual face-to-face proximity. The spread of epidemics along these interactions is simulated through an SEIR model, using both the dynamical network of contacts defined by the collected data, and two aggregated versions of such network, in order to assess the role of the data temporal aspects. We show that, on the timescales considered, an aggregated network taking into account the daily duration of contacts is a good approximation to the full resolution network, whereas a homogeneous representation which retains only the topology of the contact network fails in reproducing the size of the epidemic. These results have important implications in understanding the level of detail needed to correctly inform computational models for the study and management of real epidemics

    Real-time numerical forecast of global epidemic spreading: Case study of 2009 A/H1N1pdm

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    Background Mathematical and computational models for infectious diseases are increasingly used to support public-health decisions; however, their reliability is currently under debate. Real-time forecasts of epidemic spread using data-driven models have been hindered by the technical challenges posed by parameter estimation and validation. Data gathered for the 2009 H1N1 influenza crisis represent an unprecedented opportunity to validate real-time model predictions and define the main success criteria for different approaches. Methods We used the Global Epidemic and Mobility Model to generate stochastic simulations of epidemic spread worldwide, yielding (among other measures) the incidence and seeding events at a daily resolution for 3,362 subpopulations in 220 countries. Using a Monte Carlo Maximum Likelihood analysis, the model provided an estimate of the seasonal transmission potential during the early phase of the H1N1 pandemic and generated ensemble forecasts for the activity peaks in the northern hemisphere in the fall/winter wave. These results were validated against the real-life surveillance data collected in 48 countries, and their robustness assessed by focusing on 1) the peak timing of the pandemic; 2) the level of spatial resolution allowed by the model; and 3) the clinical attack rate and the effectiveness of the vaccine. In addition, we studied the effect of data incompleteness on the prediction reliability. Results Real-time predictions of the peak timing are found to be in good agreement with the empirical data, showing strong robustness to data that may not be accessible in real time (such as pre-exposure immunity and adherence to vaccination campaigns), but that affect the predictions for the attack rates. The timing and spatial unfolding of the pandemic are critically sensitive to the level of mobility data integrated into the model. Conclusions Our results show that large-scale models can be used to provide valuable real-time forecasts of influenza spreading, but they require high-performance computing. The quality of the forecast depends on the level of data integration, thus stressing the need for high-quality data in population-based models, and of progressive updates of validated available empirical knowledge to inform these models

    The spatial resolution of epidemic peaks

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    The emergence of novel respiratory pathogens can challenge the capacity of key health care resources, such as intensive care units, that are constrained to serve only specific geographical populations. An ability to predict the magnitude and timing of peak incidence at the scale of a single large population would help to accurately assess the value of interventions designed to reduce that peak. However, current disease-dynamic theory does not provide a clear understanding of the relationship between: epidemic trajectories at the scale of interest (e.g. city); population mobility; and higher resolution spatial effects (e.g. transmission within small neighbourhoods). Here, we used a spatially-explicit stochastic meta-population model of arbitrary spatial resolution to determine the effect of resolution on model-derived epidemic trajectories. We simulated an influenza-like pathogen spreading across theoretical and actual population densities and varied our assumptions about mobility using Latin-Hypercube sampling. Even though, by design, cumulative attack rates were the same for all resolutions and mobilities, peak incidences were different. Clear thresholds existed for all tested populations, such that models with resolutions lower than the threshold substantially overestimated population-wide peak incidence. The effect of resolution was most important in populations which were of lower density and lower mobility. With the expectation of accurate spatial incidence datasets in the near future, our objective was to provide a framework for how to use these data correctly in a spatial meta-population model. Our results suggest that there is a fundamental spatial resolution for any pathogen-population pair. If underlying interactions between pathogens and spatially heterogeneous populations are represented at this resolution or higher, accurate predictions of peak incidence for city-scale epidemics are feasible

    A combinatorial model of malware diffusion via Bluetooth connections

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    We outline here the mathematical expression of a diffusion model for cellphones malware transmitted through Bluetooth channels. In particular, we provide the deterministic formula underlying the proposed infection model, in its equivalent recursive (simple but computationally heavy) and closed form (more complex but efficiently computable) expression.Comment: In press on PlosON
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