Porcine reproductive and respiratory syndrome (PRRS) causes decreased reproductive performance in breeding animals and increased respiratory problems in growing animals, which result in significant economic losses in the swine industry.

In a paper published recently in Journal of Animal Science, N. Boddicker or Iowa State University and co-authors there and at Kansas State University, Beltsville Agricultural Research Center and New Zealand’s Massey University report that vaccination has generally not been effective in the prevention of PRRS, partially because of the rapid mutation rate and evolution of the virus.

The objective of their study was to discover the genetic basis of host resistance or susceptibility to the PRRS virus through a genome-wide association study using data from the PRRS Host Genetics Consortium PRRS-CAP project.

Three groups of approximately 190 commercial crossbred pigs from one breeding company were infected with PRRS virus between 18 and 28 days of age. Blood samples and bodyweight were collected up to 42 days post infection.

Pigs were genotyped with the Illumina Porcine 60k Beadchip. Whole-genome analysis focused on viraemia at each day blood was collected and bodyweight gains from 0 to 21 days post infection (WG21) or 42 days post infection (WG42).

Viral load (VL) was quantified as area under the curve from 0 to 21 days post infection.

Heritabilities for WG42 and VL were moderate at 0.30 and litter accounted for an additional 14 per cent of phenotypic variation.

Genomic regions associated with VL were found on chromosomes 4 and X and on 1, 4, 7 and 17 for WG42. The 1-Mb region identified on chromosome 4 influenced both WG and VL, exhibited strong linkage disequilibrium, and explained 15.7 per cent of the genetic variance for VL and 11.2 per cent for WG42.

Despite a genetic correlation of -0.46 between VL and WG42, genomic EBV for this region were favourably and nearly perfectly correlated. The favourable allele for the most significant SNP in this region had a frequency of 0.16 and estimated allele substitution effects were significant (P<0.01) for each group when the SNP was fitted as a fixed covariate in a model that included random polygenic effects with overall estimates of -4.1 units for VL (phenotypic SD=6.9) and 2.0kg (phenotypic SD=3 kg) for WG42.

Candidate genes in this region on SSC4 include the interferon induced guanylate–binding protein gene family.

Boddicker and co-authors concluded that host response to experimental PRRS virus challenge has a strong genetic component, and a QTL on chromosome 4 explains a substantial proportion of the genetic variance in the studied population.

These results could have a major impact in the pig industry by enabling marker-assisted selection to reduce the impact of PRRS but need to be validated in additional populations, the group added.

Reference

Boddicker N., E.H. Waide, R.R.R. Rowland, J.K. Lunney, D.J. Garrick, J.M. Reecy and J.C.M. Dekkers. 2012. Evidence for a major QTL associated with host response to Porcine Reproductive and Respiratory Syndrome Virus challenge. J. Anim. Sci., 90(6):1733-1746. doi: 10.2527/jas.2011-4464

Further Reading You can view the full report (fee payable) by clicking here.

Further Reading Find out more information on porcine reproductive respiratory syndrome (PRRS) by clicking here.

June 2012