Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus

Abstract

BackgroundA 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 that supports 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 to what extent 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) that were 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 to 21 (VL21) or 0 to 42 (VL42) days post-infection and tolerance as the slope of the reaction-norm of average daily gain (ADG21, ADG42) on VL21 or VL42.ResultsMulti-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 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 ADG21 or ADG42 are low to moderate.ConclusionsEvidence 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12711-017-0312-7) contains supplementary material, which is available to authorized users.

Harnessing longitudinal information to identify genetic variation in tolerance of pigs to Porcine Reproductive and Respiratory Syndrome virus infection

“…The PRRS Host Genetics Consortium (PHGC) dataset used in this study was the same as that of a previous study that provided inconclusive evidence for genetic variation in tolerance [ 10 ]. Briefly, data from 1569 commercial crossbred growing pigs supplied by various breeding companies were collected from nine PRRSV challenge trials following an identical infection protocol [ 29 ].…”

“…As in the previous tolerance study [ 10 ], only offspring from sires with more than 10 progeny with phenotypes were considered to reduce the risk of bias in tolerance estimates [ 17 ]. As such, the number of animals included was 1001 from 49 sires.…”

“…As such, the number of animals included was 1001 from 49 sires. In contrast to our previous study [ 10 ], 214 pigs that had experienced a rebound in viremia (i.e. a second period of increased serum virus load), as identified by curve fitting [ 34 ], were omitted from the analyses.…”

“…Pigs that were heterozygous AB for the WUR locus had on average 4.5% lower VL and grew on average 2 kg more over the 42-day infection period than individuals with the unfavourable AA genotype. Our previous study of the same PHGC data found inconclusive evidence for genetic variation in tolerance of pigs to PRRS, which was attributed to limited statistical power to disentangle genetic effects related to the overall growth response under infection, regardless of VL and those related to tolerance [ 10 ]. This previous study, which was based on VL and growth as single cumulative measures for each individual over time periods of 21 or 42 days, concluded that more measurements, in particularly a wider spread of individual VL measurements for fitting regression curves (e.g.…”

“…This previous study, which was based on VL and growth as single cumulative measures for each individual over time periods of 21 or 42 days, concluded that more measurements, in particularly a wider spread of individual VL measurements for fitting regression curves (e.g. including zero VL), would potentially resolve this confounding and may permit accurate estimation of genetic variance in tolerance [ 10 ].…”