Coordinatore | UNIVERSITETET I OSLO
Organization address
address: Problemveien 5-7 contact info |
Nazionalità Coordinatore | Norway [NO] |
Totale costo | 208˙353 € |
EC contributo | 208˙353 € |
Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | FP7-PEOPLE-2011-IEF |
Funding Scheme | MC-IEF |
Anno di inizio | 2012 |
Periodo (anno-mese-giorno) | 2012-04-01 - 2014-03-31 |
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1 |
UNIVERSITETET I OSLO
Organization address
address: Problemveien 5-7 contact info |
NO (OSLO) | coordinator | 208˙353.60 |
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'Yersinia pestis, the causative agent of plague, is a flea-borne disease that caused at least three devastating pandemics in the last two millenia[Stenseth08]. Plague is endemic in wildlife rodents, and the ecological and epidemiological dynamics of the rodent-plague system are the underlying cause of outbreaks in human populations. However, our current understanding of this system is insufficient to mitigate the risk. In this project the researcher will uniquely combine the disciplines of theoretical biology, molecular/evolutionary genetics, epidemiology and ecology to address this important issue.
The Centre of Ecological and Evolutionary Synthesis (CEES) in Oslo, Norway has access to unique archives on plague outbreaks in rodents and humans in Central Asia and China. These archives, and the available expertise on the genetic phylogeography of the plague at CEES, provide a great opportunity for the applicant researcher to integrate epidemiological and genetic knowledge of plague with his expertise on dynamic modelling of ecosystems. In return, CEES researchers will benefit from being exposed to these simulation models, and their application in analysing complex ecosystems, as well the contact network of the applicant researcher with modelling groups in the Netherlands and Europe. This project would both significantly strengthen plague research, and would have important corollary impacts on public health and risk assessment.
The project will use individual-based models of small rodent ecologies through which plague can spread, and observe the changes in the genetic variance of plague. These changes will be abstracted into a Cellular Automata (CA) [Hogeweg10], a modelling formalism that is suitable for simulating large ecological systems. The ecological and epidemiological dynamics of plague within the CA model will be studied in detail and under different hypothesis of plague spread, and compared against the observed genetic variance in plague in Asia.'
A study on the ecological conditions underlying plague outbreaks could aid in understanding how this and other animal-borne diseases become entrenched in a human population.
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