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ARTICLE |
1 Roslin Institute and Royal (Dick) School of Veterinary Studies, Roslin BioCentre, Midlothian, EH25 9PS, United Kingdom
* To whom correspondence should be addressed. E-mail: mintu{at}bioss.ac.uk.
| Abstract |
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The aim of this paper was to explore the impact of genetic heterogeneity in host resistance to infection, on the population-level risks and outcomes of epidemics. This was done using a stochastic epidemiological model in which the model parameters were assumed to be genetically controlled traits of the host. A finite locus model was explored, with a gene controlling the transmission coefficient (i.e., host susceptibility to infection), and a gene controlling the recovery period. Both genes were simulated to have 2 alleles with underlying additive or dominance inheritance, and independent assortment of alleles. The model was parameterized for a viral pig disease (transmissible gastroenteritis), and complete homogeneous mixing among genotypes was assumed. Mean population genotype dramatically affected epidemic outcomes, and subtle impacts of heterogeneity on epidemic properties were also observed. Genetic variation in the transmission coefficient led to probabilities of epidemics occurring that were slightly greater than expected, but genetic variation in the recovery rate had no such impact. Epidemics were generally less severe in genetically heterogeneous populations than expected from the constituent subpopulations. Furthermore, the genotype of the initial infected animal had a marked impact on epidemic probabilities, particularly when genetic variation was for recovery rate. The results of this model provide useful information to determine optimum population structures and to exploit genetic variation in resistance to infection. Applications of the proposed model in genetically heterogeneous populations for identifying practical disease management strategies are also discussed.
Key Words: animal health, disease resistance, epidemiology, genetics, infection transmission
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