Projects per year
Abstract / Description of output
Results: Multi-trait analysis of ADG associated with either low or high VL was not indicative of genetic variation in tolerance. Similarly, random regression models for ADG21and ADG42 with a tolerance slope fitted for each sire did
not result in a better fit to the data than a model without genetic variation in tolerance. However, the distribution of data around average VL suggested possible confounding between level and slope estimates of the regression lines.
Augmenting the data with simulated growth rates of non-infected half-sibs (
ADG0) helped resolve this statistical confounding and indicated that genetic variation in tolerance to PRRS may exist if genetic correlations between ADG0 and ADG21or ADG42 are low to moderate.
Conclusions: Evidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from infected piglets only. However, simulations indicated that genetic variance in tolerance may exist and could be detected if comparable data on uninfected relatives were available. In conclusion, of the two defense strategies, genetics of tolerance is more difficult to elucidate than genetics of resistance.
FingerprintDive into the research topics of 'Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus'. Together they form a unique fingerprint.
- 3 Finished
1/10/12 → 31/12/16
Tenesa, A., Archibald, A., Beard, P., Bishop, S., Bronsvoort, M., Burt, D., Freeman, T., Haley, C., Hocking, P., Houston, R., Hume, D., Joshi, A., Law, A., Michoel, T., Summers, K., Vernimmen, D., Watson, M., Wiener, P., Wilson, A., Woolliams, J., Ait-Ali, T., Barnett, M., Carlisle, A., Finlayson, H., Haga, I., Karavolos, M., Matika, O., Paterson, T., Paton, B., Pong-Wong, R., Robert, C. & Robertson, G.
1/04/12 → 31/03/17