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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 #272617
Title: A major QTL associated with host response to Porcine Reproductive and Respiratory Syndrome virus challenge

Author
item BODDICKER, N - Iowa State University
item WADE, E - Iowa State University
item ROWLAND, R - Kansas State University
item Lunney, Joan
item GARRICK, D - Iowa State University
item REECY, J - Iowa State University
item DEKKERS, J.C. - Iowa State University

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/30/2011
Publication Date: 12/28/2011
Citation: Boddicker, N., Wade, E.H., Rowland, R., Lunney, J.K., Garrick, D.J., Reecy, J., Dekkers, J.M. 2011. A major QTL associated with host response to Porcine Reproductive and Respiratory Syndrome virus challenge. Journal of Animal Science. 90:1733–1746.

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is the economically most important disease of pigs worldwide. It causes severely decreased reproductive performance in breeding animals and increased respiratory problems and morbidity in growing animals, ultimately resulting in great losses in the swine industry. Vaccination has not generally been effective in preventing PRRS, partially due to the rapid spread and evolution of the virus. The objectives of the current study was to discover the genetic basis of host resistance or susceptibility to the PRRS virus by conducting a genome wide association analysis using data generated from the PRRS Host Genetics Consortium (PHGC) and supported by the US National Pork Board and the USDA NIFA PRRS-CAP project. Data from the first 3 trials of 200 commercial crossbred pigs from one genetic source were analyzed genes that influence serum PRRS viremia and weight gain over 42 days post infection (dpi). Weaned pigs were infected with PRRS virus and blood samples and body weight data collected. Data was analyzed for heritabilities and Quantitative Trait Loci (QTL) associated with serum viral load and weight gain. To assess genetics each pig’s DNA was genotyped for 60,000 single nucleotide polymorphisms (SNPs) using the Illumina Porcine 60k Beadchip. Heritabilities for viral load and weight gain were moderate at 0.30. A genome-wide association study revealed regions on swine chromosomes (SSC) 4 and X for viral load and SSC1, 4, 7, and 17 for weight gain. In fact a 1 Mb region on SSC4 influenced both viral load and weight gain and were favorably correlated. Candidate genes on SSC4 include some associated wih interferon induced gene families. In summary, host response to experimental PRRS virus challenge has a strong genetic component. A major QTL on SSC4 explains a substantial proportion of the genetic variance of response in the studied population. These results could have a major impact in the swine industry by enabling marker-assisted selection for alleles on SSC4 associated with improved responses to PRRS. These data have been transmitted to commercial breeders associated with the PHGC for their use in improving pig genetics for selecting healthier, PRRS resistant pigs.

Technical Abstract: Porcine reproductive and respiratory syndrome (PRRS) causes severely decreased reproductive performance in breeding animals and increased respiratory problems and morbidity in growing animals, ultimately resulting in great economic losses in the swine industry. Vaccination has not generally been effective in preventing PRRS, partially due to the rapid spread and evolution of the virus. The objectives of the current study was to discover the genetic basis of host resistance or susceptibility to the PRRS virus by conducting a genome wide association analysis using data from the PRRS Host Genetics Consortium (PHGC) PRRS-CAP project. Three groups of 200 commercial crossbred pigs from one genetic source were infected with PRRS virus between 18 and 28 days of age. Blood samples and body weights were collected up to 42 days post infection (dpi). Pigs were genotyped with the Illumina Porcine 60k Beadchip. Whole genome analysis focused on viremia at each day blood was collected, and weight gains from 0 to 21 dpi (WG21) or 0 to 42 dpi (WG42). Viral load (VL) was quantified as area under the curve from 0 to 21 dpi. Heritabilities for WG and VL were moderate at 0.30, with litter effects of 0.14. Genomic regions associated with these traits were found on chromosomes (SSC) 4 and X for VL and 1, 4, 7, and 17 for WG21 and WG42. The one Mb region identified on SSC4 influenced WG and VL, exhibited strong linkage disequilibrium, and explained 15.7% of the genetic variance for VL and 11.2% for WG. Despite a moderate phenotypic correlation of -0.25 between VL and WG, genomic estimated breeding values (GEBV) for this region were perfectly and favorably correlated at -1. The favorable allele for the most significant SNP had a frequency of 0.16 and estimated allele substitution effects were significant (p<0.01) for each of the three groups when fitting the SNP as a fixed covariate along with random polygenic effects in ASREML, with estimates of -3.9, -4.7, and -4.8 units for VL (phenotypic SD = 6.9), and 3.0, 1.5, and 1.9 kg (phenotypic SD = 3 kg) for WG42. Candidate genes in this region on SSC4 include the interferon induced guanylate-binding protein gene family. In conclusion, host response to experimental PRRS virus challenge has a strong genetic component and a major QTL on SSC4 explains a substantial proportion of the genetic variance of response in the studied population. These results could have a major impact in the swine industry by enabling marker-assisted selection for improved response to PRRS.