The genetic basis of host response to experimental infection with the porcine reproductive and respiratory syndrome virus in pigs

Porcine reproductive and respiratory syndrome (PRRS) is the most economically important disease in the swine industry. The effects of PRRS are two fold in that it causes reproductive problems in breeding females and respiratory problems in growing animals. Vaccination has generally not been effective in the prevention of PRRS, partially due to the rapid mutation rate and evolution of the virus. The overall objective of this thesis was to discover the genetic basis of host response to PRRS virus (PRRSV) using data from the PRRS Host Genetics Consortium PRRS-CAP project by conducting genome-wide association analyses and estimating genetic parameters. Eight groups of ∼200 commercial crossbred pigs from 5 breeding companies and 6 unrelated populations were infected between 25 and 35 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 analyses focused on serum viremia and weight gain from 0 to 42 dpi (WG). Virus load (VL) was quantified as area under the curve of log viremia from 0 to 21 dpi. VL and WG were found to be moderately heritable at 0.44 and 0.39, respectively. A quantitative trait loci (QTL) was identified on Sus scrofa chromosome (SSC) 4 for VL and WG using data from the first 3 trials and validated in trials 4 through 8. The SSC4 QTL explained 13% of genetic variance for VL and 9% for WG. The favorable allele at the QTL had a dominance mode of action and resulted in reduced VL (0.50 phenotypic SD) and increased WG (0.49 phenotypic SD). The favorable allele was identified in all breeds represented in the trials but at a low frequency. Additional genomic regions were identified on SSCX and SSC1 for VL and SSC5 and 7 for WG, each explaining less than 3% of the genetic variance. The QTL on SSC1 was also associated with mortality in one trial where death loss was ∼50% due to secondary infections. In conclusion, host response to PRRSV infection has a sizable genetic component. Estimates of heritability were moderate and, with a frequency of 0.17 for the favorable allele for the SSC4 QTL across trials, there is opportunity for genetic improvement of pigs for response to PRRS infection.