Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Compensating for population sampling in simulations of epidemic spread on temporal contact networks.

ABSTRACT: Data describing human interactions often suffer from incomplete sampling of the underlying population. As a consequence, the study of contagion processes using data-driven models can lead to a severe underestimation of the epidemic risk. Here we present a systematic method to alleviate this issue and obtain a better estimation of the risk in the context of epidemic models informed by high-resolution time-resolved contact data. We consider several such data sets collected in various contexts and perform controlled resampling experiments. We show how the statistical information contained in the resampled data can be used to build a series of surrogate versions of the unknown contacts. We simulate epidemic processes on the resulting reconstructed data sets and show that it is possible to obtain good estimates of the outcome of simulations performed using the complete data set. We discuss limitations and potential improvements of our method.

SUBMITTER: Genois M

PROVIDER: S-EPMC4660211 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Compensating for population sampling in simulations of epidemic spread on temporal contact networks.

Génois Mathieu M Vestergaard Christian L CL Cattuto Ciro C Barrat Alain A

Nature communications 20151113

Data describing human interactions often suffer from incomplete sampling of the underlying population. As a consequence, the study of contagion processes using data-driven models can lead to a severe underestimation of the epidemic risk. Here we present a systematic method to alleviate this issue and obtain a better estimation of the risk in the context of epidemic models informed by high-resolution time-resolved contact data. We consider several such data sets collected in various contexts and ...[more]

PMID: 26563418

Similar Datasets

Relevance of temporal cores for epidemic spread in temporal networks.

Project description:Temporal networks are widely used to represent a vast diversity of systems, including in particular social interactions, and the spreading processes unfolding on top of them. The identification of structures playing important roles in such processes remains largely an open question, despite recent progresses in the case of static networks. Here, we consider as candidate structures the recently introduced concept of span-cores: the span-cores decompose a temporal network into subgraphs of controlled duration and increasing connectivity, generalizing the core-decomposition of static graphs. To assess the relevance of such structures, we explore the effectiveness of strategies aimed either at containing or maximizing the impact of a spread, based respectively on removing span-cores of high cohesiveness or duration to decrease the epidemic risk, or on seeding the process from such structures. The effectiveness of such strategies is assessed in a variety of empirical data sets and compared to baselines that use only static information on the centrality of nodes and static concepts of coreness, as well as to a baseline based on a temporal centrality measure. Our results show that the most stable and cohesive temporal cores play indeed an important role in epidemic processes on temporal networks, and that their nodes are likely to include influential spreaders.

| S-EPMC7385111 | biostudies-literature

Spread of variants of epidemic disease based on the microscopic numerical simulations on networks.

Project description:Viruses constantly undergo mutations with genomic changes. The propagation of variants of viruses is an interesting problem. We perform numerical simulations of the microscopic epidemic model based on network theory for the spread of variants. Assume that a small number of individuals infected with the variant are added to widespread infection with the original virus. When a highly infectious variant that is more transmissible than the original lineage is added, the variant spreads quickly to the wide space. On the other hand, if the infectivity is about the same as that of the original virus, the infection will not spread. The rate of spread is not linear as a function of the infection strength but increases non-linearly. This cannot be explained by the compartmental model of epidemiology but can be understood in terms of the dynamic absorbing state known from the contact process.

| S-EPMC8752609 | biostudies-literature

Epidemic spread on weighted networks.

Project description:The contact structure between hosts shapes disease spread. Most network-based models used in epidemiology tend to ignore heterogeneity in the weighting of contacts between two individuals. However, this assumption is known to be at odds with the data for many networks (e.g. sexual contact networks) and to have a critical influence on epidemics' behavior. One of the reasons why models usually ignore heterogeneity in transmission is that we currently lack tools to analyze weighted networks, such that most studies rely on numerical simulations. Here, we present a novel framework to estimate key epidemiological variables, such as the rate of early epidemic expansion (r0) and the basic reproductive ratio (R0), from joint probability distributions of number of partners (contacts) and number of interaction events through which contacts are weighted. These distributions are much easier to infer than the exact shape of the network, which makes the approach widely applicable. The framework also allows for a derivation of the full time course of epidemic prevalence and contact behaviour, which we validate with numerical simulations on networks. Overall, incorporating more realistic contact networks into epidemiological models can improve our understanding of the emergence and spread of infectious diseases.

| S-EPMC3861041 | biostudies-literature

Epidemic risk from friendship network data: an equivalence with a non-uniform sampling of contact networks.

Project description:Contacts between individuals play an important role in determining how infectious diseases spread. Various methods to gather data on such contacts co-exist, from surveys to wearable sensors. Comparisons of data obtained by different methods in the same context are however scarce, in particular with respect to their use in data-driven models of spreading processes. Here, we use a combined data set describing contacts registered by sensors and friendship relations in the same population to address this issue in a case study. We investigate if the use of the friendship network is equivalent to a sampling procedure performed on the sensor contact network with respect to the outcome of simulations of spreading processes: such an equivalence might indeed give hints on ways to compensate for the incompleteness of contact data deduced from surveys. We show that this is indeed the case for these data, for a specifically designed sampling procedure, in which respondents report their neighbors with a probability depending on their contact time. We study the impact of this specific sampling procedure on several data sets, discuss limitations of our approach and its possible applications in the use of data sets of various origins in data-driven simulations of epidemic processes.

| S-EPMC4832327 | biostudies-literature

Predicting epidemic risk from past temporal contact data.

Project description:Understanding how epidemics spread in a system is a crucial step to prevent and control outbreaks, with broad implications on the system's functioning, health, and associated costs. This can be achieved by identifying the elements at higher risk of infection and implementing targeted surveillance and control measures. One important ingredient to consider is the pattern of disease-transmission contacts among the elements, however lack of data or delays in providing updated records may hinder its use, especially for time-varying patterns. Here we explore to what extent it is possible to use past temporal data of a system's pattern of contacts to predict the risk of infection of its elements during an emerging outbreak, in absence of updated data. We focus on two real-world temporal systems; a livestock displacements trade network among animal holdings, and a network of sexual encounters in high-end prostitution. We define the node's loyalty as a local measure of its tendency to maintain contacts with the same elements over time, and uncover important non-trivial correlations with the node's epidemic risk. We show that a risk assessment analysis incorporating this knowledge and based on past structural and temporal pattern properties provides accurate predictions for both systems. Its generalizability is tested by introducing a theoretical model for generating synthetic temporal networks. High accuracy of our predictions is recovered across different settings, while the amount of possible predictions is system-specific. The proposed method can provide crucial information for the setup of targeted intervention strategies.

| S-EPMC4357450 | biostudies-literature

Individual-based approach to epidemic processes on arbitrary dynamic contact networks.

Project description:The dynamics of contact networks and epidemics of infectious diseases often occur on comparable time scales. Ignoring one of these time scales may provide an incomplete understanding of the population dynamics of the infection process. We develop an individual-based approximation for the susceptible-infected-recovered epidemic model applicable to arbitrary dynamic networks. Our framework provides, at the individual-level, the probability flow over time associated with the infection dynamics. This computationally efficient framework discards the correlation between the states of different nodes, yet provides accurate results in approximating direct numerical simulations. It naturally captures the temporal heterogeneities and correlations of contact sequences, fundamental ingredients regulating the timing and size of an epidemic outbreak, and the number of secondary infections. The high accuracy of our approximation further allows us to detect the index individual of an epidemic outbreak in real-life network data.

| S-EPMC4999888 | biostudies-other

Measurability of the epidemic reproduction number in data-driven contact networks.

Project description:The basic reproduction number is one of the conceptual cornerstones of mathematical epidemiology. Its classical definition as the number of secondary cases generated by a typical infected individual in a fully susceptible population finds a clear analytical expression in homogeneous and stratified mixing models. Along with the generation time (the interval between primary and secondary cases), the reproduction number allows for the characterization of the dynamics of an epidemic. A clear-cut theoretical picture, however, is hardly found in real data. Here, we infer from highly detailed sociodemographic data two multiplex contact networks representative of a subset of the Italian and Dutch populations. We then simulate an infection transmission process on these networks accounting for the natural history of influenza and calibrated on empirical epidemiological data. We explicitly measure the reproduction number and generation time, recording all individual-level transmission events. We find that the classical concept of the basic reproduction number is untenable in realistic populations, and it does not provide any conceptual understanding of the epidemic evolution. This departure from the classical theoretical picture is not due to behavioral changes and other exogenous epidemiological determinants. Rather, it can be simply explained by the (clustered) contact structure of the population. Finally, we provide evidence that methodologies aimed at estimating the instantaneous reproduction number can operationally be used to characterize the correct epidemic dynamics from incidence data.

| S-EPMC6294899 | biostudies-other

Revealing mechanisms of infectious disease spread through empirical contact networks.

Project description:The spread of pathogens fundamentally depends on the underlying contacts between individuals. Modeling the dynamics of infectious disease spread through contact networks, however, can be challenging due to limited knowledge of how an infectious disease spreads and its transmission rate. We developed a novel statistical tool, INoDS (Identifying contact Networks of infectious Disease Spread) that estimates the transmission rate of an infectious disease outbreak, establishes epidemiological relevance of a contact network in explaining the observed pattern of infectious disease spread and enables model comparison between different contact network hypotheses. We show that our tool is robust to incomplete data and can be easily applied to datasets where infection timings of individuals are unknown. We tested the reliability of INoDS using simulation experiments of disease spread on a synthetic contact network and find that it is robust to incomplete data and is reliable under different settings of network dynamics and disease contagiousness compared with previous approaches. We demonstrate the applicability of our method in two host-pathogen systems: Crithidia bombi in bumblebee colonies and Salmonella in wild Australian sleepy lizard populations. INoDS thus provides a novel and reliable statistical tool for identifying transmission pathways of infectious disease spread. In addition, application of INoDS extends to understanding the spread of novel or emerging infectious disease, an alternative approach to laboratory transmission experiments, and overcoming common data-collection constraints.

| S-EPMC8758098 | biostudies-literature

Dynamic contact networks of patients and MRSA spread in hospitals.

Project description:Methicillin-resistant Staphylococcus aureus (MRSA) is a difficult-to-treat infection. Increasing efforts have been taken to mitigate the epidemics and to avoid potential outbreaks in low endemic settings. Understanding the population dynamics of MRSA is essential to identify the causal mechanisms driving the epidemics and to generalise conclusions to different contexts. Previous studies neglected the temporal structure of contacts between patients and assumed homogeneous behaviour. We developed a high-resolution data-driven contact network model of interactions between 743,182 patients in 485 hospitals during 3,059 days to reproduce the exact contact sequences of the hospital population. Our model captures the exact spatial and temporal human contact behaviour and the dynamics of referrals within and between wards and hospitals at a large scale, revealing highly heterogeneous contact and mobility patterns of individual patients. A simulation exercise of epidemic spread shows that heterogeneous contacts cause the emergence of super-spreader patients, slower than exponential polynomial growth of the prevalence, and fast epidemic spread between wards and hospitals. In our simulated scenarios, screening upon hospital admittance is potentially more effective than reducing infection probability to reduce the final outbreak size. Our findings are useful to understand not only MRSA spread but also other hospital-acquired infections.

| S-EPMC7283340 | biostudies-literature

Inference of causality in epidemics on temporal contact networks.

Project description:Investigating into the past history of an epidemic outbreak is a paramount problem in epidemiology. Based on observations about the state of individuals, on the knowledge of the network of contacts and on a mathematical model for the epidemic process, the problem consists in describing some features of the posterior distribution of unobserved past events, such as the source, potential transmissions, and undetected positive cases. Several methods have been proposed for the study of these inference problems on discrete-time, synchronous epidemic models on networks, including naive Bayes, centrality measures, accelerated Monte-Carlo approaches and Belief Propagation. However, most traced real networks consist of short-time contacts on continuous time. A possibility that has been adopted is to discretize time line into identical intervals, a method that becomes more and more precise as the length of the intervals vanishes. Unfortunately, the computational time of the inference methods increase with the number of intervals, turning a sufficiently precise inference procedure often impractical. We show here an extension of the Belief Propagation method that is able to deal with a model of continuous-time events, without resorting to time discretization. We also investigate the effect of time discretization on the quality of the inference.

| S-EPMC4901330 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data