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United States Department of Agriculture

Agricultural Research Service

Research Project: PRRS CAP HOST GENETICS: CHARACTERIZATION OF HOST FACTORS THAT CONTRIBUTE TO PRRS DISEASE RESISTANCE AND SUSCEPTIBILITY

Location: Animal Parasitic Diseases

Title: Validation of a major quantitative trait locus associated with host response to experimental infection with Porcine Reproductive and Respiratory Syndrome virus

Authors
item Boddicker, Nick -
item Garrick, Dorian -
item Rowland, Raymond -
item Lunney, Joan
item Reecy, James -
item Dekkers, Jack -

Research conducted cooperatively with:
item

Submitted to: Animal Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 24, 2013
Publication Date: August 5, 2013
Citation: Boddicker, N.J., Garrick, D.J., Rowland, R.R., Lunney, J.K., Reecy, J.K., Dekkers, J.C. 2013. Validation of a major quantitative trait locus associated with host response to experimental infection with Porcine Reproductive and Respiratory Syndrome virus. Animal Genetics. DOI: 10.1111/age.12079.

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is economically the most important disease of pigs worldwide. It causes increased respiratory problems and morbidity in growing animals, and severely decreased reproductive performance in breeding animals, ultimately resulting in great losses in the swine industry. Vaccination is ineffective in preventing PRRS, partially due to the rapid spread and evolution of the virus. The objectives of the current study were to expand our studies determining the genetic basis of host resistance or susceptibility to the PRRS virus. In a previous publication (Boddicker et al., 2012) where we reported genome wide association analysis (GWAS) results using data generated from the PRRS Host Genetics Consortium (PHGC). Those results affirmed that a favorable genotype on swine chromosome 4 was associated with decreased virus load and increased weight gain, compared to the unfavorable genotype. Here we expanded that data from the first 3 to the first 5 trials of ~200 commercial crossbred pigs each from 3 different genetic sources. Data were analyzed for heritabilities and Quantitative Trait Loci (QTL) that influence serum PRRS viremia and weight gain. The validation populations consisted of 2 trials each of ~200 pigs sourced from different breeding companies and were infected with PRRS virus and followed for 42 days post infection (dpi). Across all 5 trials heritability estimates of 0.39 and 0.34 for viral load (area under the curve of log-transformed viremia from 0 to 21 dpi), and weight gain to 42 dpi, respectively. Every pig’s genomic DNA was genotyped for 60,000 single nucleotide polymorphisms (SNPs) using the Illumina Porcine 60k Beadchip. Boddicker et al., 2012 had shown that a central SNP (WUR10000125) in the chromosome 4 region could account for most of the genetic variation. For trials 4 and 5 effect estimates of SNP WUR10000125 were in the same direction and of similar magnitude as observed in the first three trials. Moreover, across all trials the 1 Mb region on chromosome 4 explained 15% of genetic variance for viral load and 11% for weight gain. The effect of the favorable minor allele at SNP WUR10000125 is dominant. Inheritance of the resistance allele by testing ordered genotypes for SNP WUR10000125 showed that the effect was present irrespective of whether the favorable allele was received from the sire or dam. In addition this resistance allele is found in major pig breeds, Landrace, Large White, Yorkshire and Duroc. In summary, pig response to experimental PRRSV challenge has a strong genetic component with a major QTL on SSC4 explaining a substantial proportion of the genetic variance. These results could have a major impact in the swine industry by enabling geneticists to develop plans for marker-assisted selection of pigs with improved response to PRRS.

Technical Abstract: Infectious diseases are costly to the swine industry and porcine reproductive and respiratory syndrome virus (PRRSV) is the most devastating. In earlier work, a quantitative trait locus associated with resistance/susceptibility to PRRSV was identified on Sus scrofa chromosome 4 (SSC4) using ~560 experimentally infected animals from a commercial cross. The favorable genotype was associated with decreased virus load and increased weight gain, compared to the unfavorable genotype. The objective here was to validate the association of the chromosome 4 region with PRRS resistance in two unrelated commercial crossbred populations. The validation populations consisted of 2 trials each of ~200 pigs sourced from different breeding companies and were infected with PRRS virus and followed for 42 days post infection. Across all 5 trials heritability estimates of 0.39 and 0.34 for viral load (area under the curve of log-transformed viremia from 0 to 21 days post infection), and weight gain to 42 days post infection, respectively. Effect estimates of SNP WUR10000125 in the chromosome 4 region were in the same direction and of similar magnitude in the two new trials as observed in the first three trials. Across all trials the 1 Mb region on chromosome 4 explained 15% of genetic variance for viral load and 11% for weight gain. The effect of the favorable minor allele at SNP WUR10000125 is dominant. Ordered genotypes for SNP WUR10000125 showed that the effect was present irrespective of whether the favorable allele was received from the sire or dam. In conclusion, selection for host response to PRRSV infection could reduce the economic impact of PRRS.

Last Modified: 4/19/2014
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