Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
33
datasets available to search
ShareScore release 0.9.0
Dataset results
33 results for “disease spread”
Disease Spread in Age Structured Populations with Maternal Age Effects
<p>Fundamental ecological processes, such as extrinsic mortality, determine population age structure. This influences disease spread when individuals of different ages differ in susceptibility or when maternal age determines offspring susceptibility. We show that Daphnia magna offspring born to young mothers are more susceptible than those born to older mothers, and consider this alongside previous observations that susceptibility declines with age in this system. We used a susceptible- infected compartmental model to investigate how age-specific susceptibility and maternal age effects on offspring susceptibility interact with demographic factors affecting disease spread. Our results show a scenario where an increase in extrinsic mortality drives an increase in transmission potential. Thus, we identify a realistic context in which age effects and maternal effects produce conditions favouring disease transmission. </p> <p>epi model R script.R</p> <p>This is the script for the SIR model as well as the associated script for life history data. </p> <p>main.body size.csv</p> <p>This is the data for the body size data collected in the main experiment. This was measured using imageJ, was recorded in pixels and converted into millimetres. </p> <p>main.exposed.csv</p> <p>This is the proportion of infected/not infected individuals from an exposed treatment group. This was a subset of individuals from the entire experiment. This was the result of the exposures from the main experiment. </p> <p>main.reproduction.csv</p> <p>This document records reproduction for individuals from old or young mothers. It is a count of the offspring born at each reproductive event, which occurs generally every three days, though variation in interclutch interval increases with age. This was from the main experiment. Only those who were unexposed to the parasite, where used for this portion of the experimental work. </p> <p>sm.body size.csv</p> <p>This records body size similarly to above, and was an independent replication of the main experiment. </p> <p>sm.infection status.csv</p> <p>This is infection outcomes of exposures carried out as above, in an independent replication of the main experiment. </p> <p>sm.total babies.csv</p> <p>This is the reproductive output, carried out similarly to above, but in an independent replication of the main experiment. </p>
Synaptic oligomeric tau in Alzheimer's disease – a potential culprit in the spread of tau pathology through the brain
<p>In Alzheimer’s disease (AD), fibrillar tau pathology accumulates and spreads through the brain and synapses are lost. Evidence from mouse models indicates that tau spreads trans-synaptically from pre- to postsynapses and that oligomeric tau is synaptotoxic, but data on synaptic tau in human brain is scarce. Here we used sub-diffraction-limit microscopy to study synaptic tau accumulation in post-mortem temporal and occipital cortices of human AD and control donors. Oligomeric tau is present in both pre- and postsynaptic terminals even in areas without abundant fibrillar tau deposition. Further, there is a higher proportion of oligomeric tau compared to phosphorylated or misfolded tau found at synaptic terminals. These data suggest that accumulation of oligomeric tau in synapses is an early event in disease pathogenesis, and that tau pathology may progress through the brain via trans-synaptic spread in human disease. Thus, specifically reducing oligomeric tau at synapses may be a promising therapeutic strategy for AD.</p>
The last moves: the effect of hunting and culling on the risk of disease spread from a population of reindeer
<p>1. Hunting and culling are frequently used to combat infectious wildlife diseases. The aim is to markedly lower population density in order to limit disease transmission or to eradicate the host. Massive host culling can yield a trade-off when combating wildlife disease; it follows that intrusive actions may have unintended behavioural side-effects, leading to the geographic spread of disease. The manner in which such excessive hunting and culling of hosts can affect the movement and dispersion of cervids has not been studied.</p> <p>2. In this study, we quantified the behaviour (daily movements and habitat use) and dispersion of GPS-marked reindeer (n = 24) before and during the eradication of an entire population (>2000 reindeer) infected with chronic wasting disease (CWD) in Norway. We compared behaviour and dispersion during 10 ordinary hunting seasons (2007-16), an extended hunt in 2017 and marksmen culling (2017/18).</p> <p>3. Seasonality had a major impact on movements. Reindeer movements during the early hunting season (20 August–20 September) did not increase the overall movements compared to that in the pre-hunt season (20 July–19 August), while extended hunting into October (as in 2017) and marksmen culling from November to February markedly increased daytime movements relative to that normally observed in this time of the year. Towards the end of the eradication, the remaining reindeer sought refuge at restricted high-elevation areas with limited forage production. Reindeer used novel areas towards the perimeter of the range, but active herding during culling stopped one herd from leaving the CWD zone.</p> <p>4. Synthesis and applications: With emerging wildlife diseases, host culling is becoming a more frequently used tool for managers in Europe. Our study highlights the potential trade-off between combating disease transmission within a population and the risk of geographic spread. Such insight is important to design mitigation measures, such as perimeter fencing or herding, to avoid the risk of the geographic spread of disease in cases of severe and economically important wildlife diseases.</p>
Data and code from: Vector demography, dispersal, and the spread of disease: Experimental epidemics under elevated resource supply
1. The spread of many diseases depends on the demography and dispersal of arthropod vectors. Classic epidemiological theory typically ignores vector dynamics and instead makes the simplifying assumption of frequency-dependent transmission. Yet vector ecology may be critical for understanding the spread of disease over space and time and how disease dynamics respond to environmental change. 2. Here, we ask how environmental change shapes vector demography and dispersal, and how these traits of vectors govern the spatiotemporal spread of disease. 3. We developed disease models parameterized by traits of vectors and fit them to experimental epidemics. The experiment featured a viral pathogen (CYDV-RPV) vectored by aphids (Rhopalosiphum padi) among populations of grass hosts (Avena sativa) under two rates of environmental resource supply (i.e., fertilization of the host). We compared a non-spatial model that ignores vector movement, a lagged dispersal model that emphasizes the delay between vector reproduction and dispersal, and a travelling wave model that generates waves of infections across space and time. 4. Resource supply altered both vector demography and dispersal. The lagged dispersal model fit best, indicating that vectors first reproduced and then dispersed among hosts in the experiment. Elevated resources decreased vector population growth rates, nearly doubled their carrying capacity per host, increased dispersal rates when vectors carried the virus, and homogenized disease risk across space. 5. Together, the models and experiment show how environmental eutrophication can shape spatial disease dynamics – for example, homogenizing disease risk across space – by altering the demography and behavior of vectors.
Replication files for: Integrative modeling of the spread of serious infectious diseases and corresponding wastewater dynamics
<p>This repository contains the inputs used and outputs produced by the urban water management modelling software ++SYSTEMS for the paper Integrative Modeling of the Spread of Serious Infectious Diseases and Corresponding Wastewater Dynamics. It includes the following files:</p> <ol> <li>simulation_output.zip:</li> <ol> <li>In the subfolder infection_model, .csv and .txt files containing the agent-based model outputs for 250 simulations with homogeneous infection initialisation (2024_09_17) or localised infection initialisation (2024_10_15). These files were used as inputs for ++SYSTEMS.</li> <li>In the subfolder wastewater_model, .txt files containing the flow rates by pipe and the viral concentrations by sampling location for each combination of ABM simulation and rain/decay scenario. These files were the outputs of ++SYSTEMS.</li> </ol> <li>S1_INSIDe_Demonstrator_AreaList.txt: .txt file defining the area types and number of inhabitants for each surface area within the synthetic neighbourhood used in the paper. This file was also used as an input for ++SYSTEMS.<span> </span></li> <li>S2_systems_model_files.zip: .csv files defining the characteristics of the sewage system for the synthetic neighbourhood as well as the rain scenarios used in the paper. These file were also used as inputs for ++SYSTEMS.<span> </span></li> </ol>
The last moves: the effect of hunting and culling on the risk of disease spread from a population of reindeer
Open the record for dataset details and reuse information.
Data and code from: Vector demography, dispersal, and the spread of disease: Experimental epidemics under elevated resource supply
Open the record for dataset details and reuse information.
Data from: Pathogens manipulate the preference of vectors, slowing disease spread in a multi-host system
The spread of vector‐borne pathogens depends on a complex set of interactions among pathogen, vector, and host. In single‐host systems, pathogens can induce changes in vector preferences for infected vs. healthy hosts. Yet it is unclear if pathogens also induce changes in vector preference among host species, and how changes in vector behaviour alter the ecological dynamics of disease spread. Here, we couple multi‐host preference experiments with a novel model of vector preference general to both single and multi‐host communities. We show that viruliferous aphids exhibit strong preferences for healthy and long‐lived hosts. Coupling experimental results with modelling to account for preference leads to a strong decrease in overall pathogen spread through multi‐host communities due to non‐random sorting of viruliferous vectors between preferred and non‐preferred host species. Our results demonstrate the importance of the interplay between vector behaviour and host diversity as a key mechanism in the spread of vectored‐diseases.
Data from: Infection-induced behavioural changes reduce connectivity and the potential for disease spread in wild mice contact networks
Infection may modify the behaviour of the host and of its conspecifics in a group, potentially altering social connectivity. Because many infectious diseases are transmitted through social contact, social connectivity changes can impact transmission dynamics. Previous approaches to understanding disease transmission dynamics in wild populations were limited in their ability to disentangle different factors that determine the outcome of disease outbreaks. Here we ask how social connectivity is affected by infection and how this relationship impacts disease transmission dynamics. We experimentally manipulated disease status of wild house mice using an immune challenge and monitored social interactions within this free-living population before and after manipulation using automated tracking. The immune-challenged animals showed reduced connectivity to their social groups, which happened as a function of their own behaviour, rather than through conspecific avoidance. We incorporated these disease-induced changes of social connectivity among individuals into models of disease outbreaks over the empirically-derived networks. The models revealed that changes in host behaviour frequently resulted in the disease being contained to very few animals, as opposed to becoming widespread. Our results highlight the importance of considering the role that behavioural alterations during infection can have on social dynamics when evaluating the potential for disease outbreaks.
Data from: Disentangling the drivers of invasion spread in a vector-borne tree disease
1. Pine wilt disease (PWD) invaded southern Japan in the early 1900's and has gradually expanded its range to northern Honshu (Japanese mainland). The disease is caused by a pathogenic North American nematode, which is transmitted by native pine sawyer beetles. Recently the disease has invaded other portions of East Asia and Europe where extensive mortality of host pines is anticipated to resemble historical patterns seen in Japan. 2. There is a critical need to identify the main drivers of PWD invasion spread so as to predict future spread and evaluate containment strategies in newly invaded world regions. But the coupling of pathogen and vector population dynamics introduces considerable complexity that is important for understanding this and other plant disease invasions. 3. In this study, we analysed historical (1980-2011) records of PWD infection and vector abundance, which were spatially extensive but recorded at coarse categorical levels (none, low and high) across 403 municipalities in northern Honshu. We employed a multistate occupancy model that accounted both for demographic stochasticity and observation errors in categorical data. 4. Analysis revealed that sparse sawyer populations had lower probabilities of transition to high abundance than did more abundant populations even when regional abundance stayed the same, suggesting the existence of positive density dependence, i.e. an Allee effect, in sawyer dynamics. Climatic conditions (average accumulated degree days) substantially limited invasion spread in northern regions, but this climatic influence on sawyer dynamics was generally weaker than the Allee effect. 5. Our results suggest that tactics (e.g., sanitation logging of infected pines) which strengthen Allee effects in sawyer dynamics may be effective strategies for slowing the spread of PWD.
Codes: An early warning indicator trained on stochastic disease-spreading models with different noises
<p>This dataset contains the training data (Version V1) and all the codes (Version V2) of the paper entitled "An early warning indicator trained on stochastic disease-spreading models with different noises." </p> <p>Time series and corresponding residuals from white noise (equation 2.5), environmental noise (equation 2.8), and demographic noise (equation 2.9) are stored in the training_data_WhiteN, training_data_EnvN, and training_data_DemN folders, respectively. All residuals of the time series are contained in the training_resids folder, which also includes labels and groups of the training data. For details on the data generation process, please refer to section 3.1 in the paper. </p>
Data for: Can pharmaceutical pollution alter the spread of infectious disease? A case study using fluoxetine.
<p>Human activity is changing global environments at an unprecedented rate, imposing new ecological and evolutionary ramifications on wildlife dynamics, including host-parasite interactions. Here we investigate how an emerging concern of modern human activity, pharmaceutical pollution, influences the spread of disease in a population, using the water flea <em>Daphnia</em> <em>magna</em> and the bacterial pathogen <em>Pasteuria</em> <em>ramosa</em> as a model system. We found that exposure to different concentrations of fluoxetine—a widely prescribed psychoactive drug and widespread contaminant of aquatic ecosystems—affected the severity of disease experienced by an individual in a non-monotonic manner. The direction and magnitude of any effect, however, varied with both the infection outcome measured, as well as the genotype of the pathogen. In contrast, the characteristics of unexposed animals, and thus the growth and density of susceptible hosts, were robust to fluoxetine. Using our data to parameterise an epidemiology model, we show that fluoxetine is unlikely to lead to a net increase or decrease in the likelihood of an infectious disease outbreak, as measured by a pathogen's transmission rate or basic reproductive number. Instead, any given pathogen genotype may experience a two-fold change in likely fitness, but often in opposing directions. Our study demonstrates that changes in pharmaceutical pollution give rise to complex genotype-by-environment interactions in its influence on disease dynamics, with repercussions on pathogen genetic diversity and evolution.</p>
Data from: Pathogens manipulate the preference of vectors, slowing disease spread in a multi-host system
Open the record for dataset details and reuse information.
Data from: Disentangling the genetic origins of a plant pathogen during disease spread using an original molecular epidemiology approach
Open the record for dataset details and reuse information.
Data from: Reconstructing the emergence of a lethal infectious disease of wildlife supports a key role for spread through translocations by humans
Open the record for dataset details and reuse information.
Data from: Disentangling the drivers of invasion spread in a vector-borne tree disease
Open the record for dataset details and reuse information.
Genetic testing limits the spread of inherited kidney disease while avoiding inbreeding in domestic cats
Open the record for dataset details and reuse information.
Data from: Degree of host susceptibility in the initial disease outbreak influences subsequent epidemic spread
Open the record for dataset details and reuse information.
Data for: Can pharmaceutical pollution alter the spread of infectious disease? A case study using fluoxetine.
Open the record for dataset details and reuse information.
Data from: Infection-induced behavioural changes reduce connectivity and the potential for disease spread in wild mice contact networks
Open the record for dataset details and reuse information.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.