@misc{siva-jothy_population-level_2019,
	title = {Population-{Level} {Disease} {Dynamics} {Reflect} {Individual} {Heterogeneities} in {Transmission}},
	copyright = {© 2019, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0, as described at http://creativecommons.org/licenses/by-nd/4.0/},
	url = {https://www.biorxiv.org/content/10.1101/735480v1},
	doi = {10.1101/735480},
	abstract = {Host heterogeneity in disease transmission is widespread and presents a major hurdle to predicting and minimizing pathogen spread. Using the Drosophila melanogaster model system infected with Drosophila C virus, we integrate experimental measurements of individual host heterogeneity in social aggregation, virus shedding, and disease-induced mortality into an epidemiological framework that simulates outbreaks of infectious disease. We use these simulations to calculate individual variation in disease transmission and apportion this variation to specific components of transmission: social network degree distribution, infectiousness, and infection duration. The experimentally-observed variation produces substantial differences in individual transmission potential, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. Manipulating variation in social network connectivity, infectiousness, and infection duration in simulated populations reveals that these components affect disease transmission in clear and distinct ways. We consider the implications of this genetic and sex-specific variation in disease transmission and discuss implications for appropriate control methods given the relative contributions made by social aggregation, virus shedding, and infection duration to transmission in other host-pathogen systems.},
	language = {en},
	urldate = {2024-06-04},
	publisher = {bioRxiv},
	author = {Siva-Jothy, Jonathon A. and White, Lauren A. and Craft, Meggan E. and Vale, Pedro F.},
	month = aug,
	year = {2019},
	note = {Pages: 735480
Section: New Results},
}

{"_id":"L7eiJskj9beguxds6","bibbaseid":"sivajothy-white-craft-vale-populationleveldiseasedynamicsreflectindividualheterogeneitiesintransmission-2019","author_short":["Siva-Jothy, J. A.","White, L. A.","Craft, M. E.","Vale, P. F."],"bibdata":{"bibtype":"misc","type":"misc","title":"Population-Level Disease Dynamics Reflect Individual Heterogeneities in Transmission","copyright":"© 2019, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0, as described at http://creativecommons.org/licenses/by-nd/4.0/","url":"https://www.biorxiv.org/content/10.1101/735480v1","doi":"10.1101/735480","abstract":"Host heterogeneity in disease transmission is widespread and presents a major hurdle to predicting and minimizing pathogen spread. Using the Drosophila melanogaster model system infected with Drosophila C virus, we integrate experimental measurements of individual host heterogeneity in social aggregation, virus shedding, and disease-induced mortality into an epidemiological framework that simulates outbreaks of infectious disease. We use these simulations to calculate individual variation in disease transmission and apportion this variation to specific components of transmission: social network degree distribution, infectiousness, and infection duration. The experimentally-observed variation produces substantial differences in individual transmission potential, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. Manipulating variation in social network connectivity, infectiousness, and infection duration in simulated populations reveals that these components affect disease transmission in clear and distinct ways. We consider the implications of this genetic and sex-specific variation in disease transmission and discuss implications for appropriate control methods given the relative contributions made by social aggregation, virus shedding, and infection duration to transmission in other host-pathogen systems.","language":"en","urldate":"2024-06-04","publisher":"bioRxiv","author":[{"propositions":[],"lastnames":["Siva-Jothy"],"firstnames":["Jonathon","A."],"suffixes":[]},{"propositions":[],"lastnames":["White"],"firstnames":["Lauren","A."],"suffixes":[]},{"propositions":[],"lastnames":["Craft"],"firstnames":["Meggan","E."],"suffixes":[]},{"propositions":[],"lastnames":["Vale"],"firstnames":["Pedro","F."],"suffixes":[]}],"month":"August","year":"2019","note":"Pages: 735480 Section: New Results","bibtex":"@misc{siva-jothy_population-level_2019,\n\ttitle = {Population-{Level} {Disease} {Dynamics} {Reflect} {Individual} {Heterogeneities} in {Transmission}},\n\tcopyright = {© 2019, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0, as described at http://creativecommons.org/licenses/by-nd/4.0/},\n\turl = {https://www.biorxiv.org/content/10.1101/735480v1},\n\tdoi = {10.1101/735480},\n\tabstract = {Host heterogeneity in disease transmission is widespread and presents a major hurdle to predicting and minimizing pathogen spread. Using the Drosophila melanogaster model system infected with Drosophila C virus, we integrate experimental measurements of individual host heterogeneity in social aggregation, virus shedding, and disease-induced mortality into an epidemiological framework that simulates outbreaks of infectious disease. We use these simulations to calculate individual variation in disease transmission and apportion this variation to specific components of transmission: social network degree distribution, infectiousness, and infection duration. The experimentally-observed variation produces substantial differences in individual transmission potential, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. Manipulating variation in social network connectivity, infectiousness, and infection duration in simulated populations reveals that these components affect disease transmission in clear and distinct ways. We consider the implications of this genetic and sex-specific variation in disease transmission and discuss implications for appropriate control methods given the relative contributions made by social aggregation, virus shedding, and infection duration to transmission in other host-pathogen systems.},\n\tlanguage = {en},\n\turldate = {2024-06-04},\n\tpublisher = {bioRxiv},\n\tauthor = {Siva-Jothy, Jonathon A. and White, Lauren A. and Craft, Meggan E. and Vale, Pedro F.},\n\tmonth = aug,\n\tyear = {2019},\n\tnote = {Pages: 735480\nSection: New Results},\n}\n\n\n\n","author_short":["Siva-Jothy, J. A.","White, L. A.","Craft, M. E.","Vale, P. F."],"key":"siva-jothy_population-level_2019","id":"siva-jothy_population-level_2019","bibbaseid":"sivajothy-white-craft-vale-populationleveldiseasedynamicsreflectindividualheterogeneitiesintransmission-2019","role":"author","urls":{"Paper":"https://www.biorxiv.org/content/10.1101/735480v1"},"metadata":{"authorlinks":{}}},"bibtype":"misc","biburl":"https://bibbase.org/zotero-mypublications/pfvale","dataSources":["Hmaj6fS6FKQuG3nSG","tWbkRzQp4qoRJ9g7W","WhdFcL9q2Loo6bDrg","rf5D6MWTahxXEXZ5P","66wkvtmTF9APhQn6L"],"keywords":[],"search_terms":["population","level","disease","dynamics","reflect","individual","heterogeneities","transmission","siva-jothy","white","craft","vale"],"title":"Population-Level Disease Dynamics Reflect Individual Heterogeneities in Transmission","year":2019}