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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Parasitic Diseases Laboratory » Research » Publications at this Location » Publication #298976
Title: Genome-wide association and genomic prediction for host response to Porcine Reproductive and Respiratory Syndrome infection

Author
item BODDICKER, N - Iowa State University
item BJORKQUIST, A - Iowa State University
item ROWLAND, R - Kansas State University
item Lunney, Joan
item REECY, J - Iowa State University
item DEKKERS, JC - Iowa State University

Submitted to: Genetics Selection Evolution
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/13/2013
Publication Date: 3/4/2014
Citation: Boddicker, N., Bjorkquist, A., Rowland, R.R., Lunney, J.K., Reecy, J.M., Dekkers, J.M. 2014. Genome-wide association and genomic prediction for host response to Porcine Reproductive and Respiratory Syndrome infection. Genetics Selection Evolution. 46:18.

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 objective of the current study was to expand our studies determining the genetic basis of host resistance or susceptibility to the PRRS virus. In our previous publications (Boddicker et al., 2012; 2013) we reported genome wide association analysis (GWAS) results using data generated from the PRRS Host Genetics Consortium (PHGC), a national effort to assess the role of genetics in determining pig resistance/susceptibility to PRRS virus infection and related pathology and growth effects. We previously showed that a favorable genotype on swine chromosome 4 (SSC4) was associated with decreased virus load and increased weight gain, compared to the unfavorable genotype. With this manuscript we affirmed that heritability estimates were 0.44 and 0.29 for viral load (VL) to 21 days post infection and weight gain to 42 days post infection (WG), respectively. Genomic regions associated with VL were identified on chromosomes 4, X, and 1. Genomic regions associated with WG were identified on chromosomes 4, 5, and 7. Apart from the SSC4 region, each of these chromosomal regions explained less than 3% of the genetic variance (as compared to 15% and 11% for VL and WG for SSC4). The accuracies of genomic estimated breeding values based on the SSC4 region were high (0.55), while the rest of the genome had little predictive ability across populations (0.09). Overall, traits associated with response to PRRSV infection are largely controlled by genomic regions with relatively small effects, with the exception of SSC4. These results show that selection for the SSC4 region could reduce the effects of PRRS, ultimately reducing the economic impact of this disease. 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: Background: Host genetics has been shown to play a role in porcine reproductive and respiratory syndrome (PRRS), which is the most economically important disease to the swine industry. A region on Sus scrofa chromosome (SSC) 4 has been previously reported to have a strong association with serum viremia and weight gain in pigs experimentally infected with the PRRS virus (PRRSV). The objective here was to identify haplotypes associated with the favorable phenotype, investigate additional genomic regions associated with host response to PRRSV, and to determine the predictive ability of genomic estimated breeding values (GEBV) based on the SSC4 region and based on the rest of the genome. Phenotypic data and 60K SNP genotypes from 8 trials of ~200 pigs from different commercial crosses were used to address these objectives. Results: Across the 8 trials, heritability estimates were 0.44 and 0.29 for viral load (VL, area under the curve of log-transformed serum viremia from 0 to 21 days post infection) and weight gain to 42 days post infection (WG), respectively. Genomic regions associated with VL were identified on chromosomes 4, X, and 1. Genomic regions associated with WG were identified on chromosomes 4, 5, and 7. Apart from the SSC4 region, the regions associated with these 2 traits each explained less than 3% of the genetic variance. Due to the strong linkage disequilibrium in the SSC4 region, only 19 unique haplotypes were identified across all populations, of which 4 were associated with the favorable phenotype. Through cross validation, accuracies of EBV based on the SSC4 region were high (0.55), while the rest of the genome had little predictive ability across populations (0.09). Conclusions: Traits associated with response to PRRSV infection are largely controlled by genomic regions with relatively small effects, with the exception of SSC4. Accuracies of EBVs based on the SSC4 region were high compared to the rest of the genome. These results show that selection for the SSC4 region could reduce the effects of PRRS, ultimately reducing the economic impact of this disease.