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 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.
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 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.
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.
|Number of pages||15|
|Journal||Genetics Selection Evolution|
|Publication status||Published - 19 Apr 2017|
Bibliographical noteFunding Information:
This study was funded by the BBSRC and Genus within the remit of a BBSRC Industrial Case Ph.D. studentship (GL) and BBSRC Institute Strategic Pro‑ gramme Grant to ABD‑W (ISP1, BB/J004235/1, Theme 5 BBS/E/D/20211554). IK received funding from the Higher Education Funding Council for England (HEFCE). HR was funded by Marie Curie Initial Training Networks (FP7‑People‑ 2010‑ITN) as part of the NematodeSystemHealth project, and co‑financed by Topigs Norsvin, the Netherlands, and Dutch Ministry of Economic Affairs, Agriculture, and Innovation (Public–private partnership “Breed4Food”Code KB‑12‑006.03‑004‑ASG‑LR and KB‑12‑006.03‑005‑ASG‑LR).
The authors would like to thank the PRRS Host Genetic Consortium for access and use of the dataset. The PHGC was supported by US National Pork Board Grants, USDA NIFA Awards (2008‑55620‑19132, 2010‑65205‑20433, 2013‑ 68004‑20362), and pig breeding companies, consisting of PIC/Genus, Choice Genetics, Fast Genetics, Genesus, Inc., TopigsNorsvin, and PigGen Canada, Inc., that provided the pigs for the study.
© 2017 The Author(s).
ASJC Scopus subject areas
- Ecology, Evolution, Behavior and Systematics
- Animal Science and Zoology