Effect of a genetic marker for the GBP5 gene on resilience to a polymicrobial natural disease challenge in pigs

A genomic region on chromosome 4 that is tagged by single nucleotide polymorphism (SNP) WUR0000125 (WUR) was previously found to be associated with host response to porcine reproductive and respiratory syndrome (PRRS) virus infection. The objectives of this study were to 1) determine whether genotype at the WUR SNP is also associated with resilience to a natural polymicrobial disease challenge, 2) investigate the relationship of genotype at the WUR SNP with genotype at its putative causative mutation in the GBP5 gene, and 3) compare the association of the WUR and GBP5 SNPs with host response to PRRS virus infection. Data from two studies were used: 1) Eight trials of the PRRS Host Genetic Consortium, in which ~200 naïve crossbred nursery pigs per trial were infected with the NVSL-97-7895 strain of PRRS to study the effects of genotype at the GBP5 and WUR SNPs on viral load and weight gain post-infection; 2) a natural disease challenge, where 3139 naïve crossbred nursery barrows were entered into a grow-finish facility that was seeded with multiple pathogens to maximize expression of disease resilience. Results from the PRRS trials showed that the WUR and GBP5 SNPs are in high but not complete linkage disequilibrium (r2 = 0.94). A haplotype analysis showed that discordant genotypes between the WUR and GBP5 SNPs were due to genetic recombination and not the result of genotyping errors. We had insufficient statistical power to determine whether the GBP5 or WUR SNP had a stronger effect on phenotype. Results from the natural disease challenge indicated that the favorable allele for the WUR SNP was significantly associated with greater average daily gain (p = 0.02) and with lower numbers of treatments in the challenge nursery (p = 0.05) and across the nursery and finisher (p = 0.01). Therefore, swine breeders can continue to use the WUR SNP not only as a marker for resilience to PRRS but also as a marker for disease resilience to a polymicrobial disease challenge, although its linkage disequilibrium with the putative causative mutation in the GBP5 gene must continue to be monitored.