Using multi-trait and random regression models to identify genetic variation in tolerance of pigs to Porcine Reproductive and Respiratory Syndrome virus

Authors: LOUGH, GRAHAM - Roslin Institute; RASHIDI, HAMED - Wageningen University; KYRIAZAKIS, ILIAS - Newcastle University; DEKKERS, JACK - Iowa State University; HESS, ANDREW - Iowa State University; HESS, MELANIE - Iowa State University; DEEB, NADER - Genus; KAUSE, ANTTI - Natural Resources Institute Finland (LUKE); Lunney, Joan; ROWLAND, RAYMOND - Kansas State University; MULDER, HAN - Wageningen University; DOESCHL-WILSON, ANDREA - Roslin Institute

Submitted to: Genetics Selection Evolution
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/29/2017
Publication Date: 4/19/2017
Citation: Lough, G., Rashidi, H., Kyriazakis, I., Dekkers, J.C., Hess, A.S., Hess, M.K., Deeb, N., Kause, A., Lunney, J.K., Rowland, R.R., Mulder, H., Doeschl-Wilson, A. 2017. Using multi-trait and random regression models to identify genetic variation in tolerance of pigs to Porcine Reproductive and Respiratory Syndrome virus. Genetics Selection Evolution. 49:37.

Interpretive Summary: This paper addresses important differences in host responses to infection: does an animal survive an infection due to resistance (reduced pathogen load) and/or due to tolerance (lower impact of infection on performance). Both response strategies may be under genetic control and could thus be targets for use for genetic improvement of livestock. Our past work has provided evidence in support of a genetic basis for resistance to Porcine Reproductive and Respiratory Syndrome (PRRS). However, it was not known whether pigs also differed genetically in tolerance PRRS virus infection. We determined the extent to which pigs that have been shown to vary genetically in resistance to PRRS also exhibit genetic variation in tolerance. Evidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from only infected piglets. However, simulations indicated that genetic variance in tolerance may exist and could be detected if comparable data on uninfected relatives were available. We concluded that unlike the proven genetics of resistance to PRRS virus infection, genetics of tolerance can be predicted but will be more difficult to verify.

Technical Abstract: Background A host can adopt two response strategies to infection: resistance (reduce pathogen load) and tolerance (minimize impact of infection on performance). Both strategies may be under genetic control and could thus be targeted for genetic improvement. Although there is evidence in support of a genetic basis for resistance to Porcine Reproductive and Respiratory Syndrome (PRRS), it is not known whether pigs also differ genetically in tolerance. We determined the extent to which pigs that have been shown to vary genetically in resistance to PRRS also exhibit genetic variation in tolerance. Multi-trait linear mixed models and random regression sire models were fitted to PRRS Host Genetics Consortium data from 1320 weaned pigs (offspring of 54 sires) experimentally infected with a virulent strain of PRRS virus to obtain genetic parameter estimates for resistance and tolerance. Resistance was defined as the inverse of within-host viral load (VL) from 0-21 (VL21) or 0-42 (VL42) days post infection and tolerance as the slope of the reaction-norm of average daily gain (ADG21, ADG42) on VL21 or VL42. 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 ADG21 and 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 intercept 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 genetic variation in tolerance to PRRS may exist if genetic correlations between ADG0 and ADG21 or ADG42 are low to moderate. Conclusions Evidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from only infected piglets. 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 defence strategies, genetics of tolerance is more difficult to elucidate than genetics of resistance.