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

Abstract

BackgroundHigh resistance (the ability of the host to reduce pathogen load) and tolerance (the ability to maintain high performance at a given pathogen load) are two desirable host traits for producing animals that are resilient to infections. For Porcine Reproductive and Respiratory Syndrome (PRRS), one of the most devastating swine diseases worldwide, studies have identified substantial genetic variation in resistance of pigs, but evidence for genetic variation in tolerance has so far been inconclusive. Resistance and tolerance are usually considered as static traits. In this study, we used longitudinal viremia measurements of PRRS virus infected pigs to define discrete stages of infection based on viremia profile characteristics. These were used to investigate host genetic effects on viral load (VL) and growth at different stages of infection, to quantify genetic variation in tolerance at these stages and throughout the entire 42-day observation period, and to assess whether the single nucleotide polymorphism (SNP) WUR10000125 (WUR) with known large effects on resistance confers significant differences in tolerance.ResultsGenetic correlations between resistance and growth changed considerably over time. Individuals that expressed high genetic resistance early in infection tended to grow slower during that time-period, but were more likely to experience lower VL and recovery in growth by the later stage. The WUR genotype was most strongly associated with VL at early- to mid-stages of infection, and with growth at mid- to late-stages of infection. Both, single-stage and repeated measurements random regression models identified significant genetic variation in tolerance. The WUR SNP was significantly associated only with the overall tolerance slope fitted through all stages of infection, with the genetically more resistant AB pigs for the WUR SNP being also more tolerant to PRRS.ConclusionsThe results suggest that genetic selection for improved tolerance of pigs to PRRS is possible in principle, but may be feasible only with genomic selection, requiring intense recording schemes that involve repeated measurements to reliably estimate genetic effects. In the absence of such records, consideration of the WUR genotype in current selection schemes appears to be a promising strategy to improve simultaneously resistance and tolerance of growing pigs to PRRS.Electronic supplementary materialThe online version of this article (10.1186/s12711-018-0420-z) contains supplementary material, which is available to authorized users.

Genetically determined resistance and tolerance to Diplostomum sp. parasite in farmed rainbow trout

“…Based on these results, it might be a good optional strategy for a host fish not to combat with parasites but to put the effort on tolerance, that is, maximize fitness despite the parasites. In theory, this could mean allocating resources to growth and feeding virus (Lough et al, 2018). In fish, genetic variation in the amount of fin erosion caused by parasite Tracheliastes polycolpus (Crustacea:…”

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“…This has been exemplified for PRRS, where GWAS identified a region on pig chromosome 4 with a major QTL that explained 10 to 20% of the genetic variance for resistance and resilience to PRRS [85]. Subsequent studies found that this QTL is also significantly associated with tolerance to PRRS, with the genetically more resistant pigs being also more tolerant [32]. Selection on such QTL with known beneficial pleiotropic effects on both traits may be a promising short-term strategy to gradually improve resistance and tolerance simultaneously in the absence of reliable genetic correlation estimates.…”

“…Estimates can be derived by applying the above model to data from a large scale PRRS virus challenge experiment where piglets were infected with the same dose of a virulent PRRS virus strain at about 30 days of age [31]. Lough et al [32] derived tolerance estimates from individual body weight and viremia records on 1011 of these young pigs by linear regression of performance on within-host PL. Here, performance was the average growth rate from 14 to 42 days post-infection; pathogen load was AUC(logVL), i.e.…”

“…b The associated reaction norms and dynamic resilience trajectories. Data from[32]. Datapoints represent observations (the earliest ones as open symbols, the final ones as arrowheads), the solid trendlines in (b) show time trends.…”

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“…The losses from PRRS are estimated at $2.5 billion per annum in the USA and Europe alone. Quantitative genetics studies have identified substantial genetic variation in the resistance and tolerance of pigs to PRRS [ 85 , 86 ], with a single locus on pig chromosome 4 ( GBP5 , encoding guanylate-binding protein 5) explaining 15% of the total genetic variation in viral load and 11% of genetic variation for growth rate in pigs infected with PRRSV [ 87 , 88 ]. Although these results could offer promising opportunities for mitigating PRRS through genomic selection, predicting the impact of genomic selection on PRRS prevalence is difficult as the role of the GBP5 locus in PRRS transmission is currently not known.…”