Comparison of host genetic factors influencing pig response to infection with two North American isolates of porcine reproductive and respiratory syndrome virus

Abstract

BackgroundPorcine reproductive and respiratory syndrome (PRRS) is one of the most important swine diseases in the world and genetic selection of pigs for increased resistance to PRRS is an attractive method to improve the health status of the swine herd. This study compared phenotypic and genetic responses to infection with one of two genetically distinct type 2 PRRS virus (PRRSV) isolates: NVSL-97-7895 (NVSL) and KS-2006-72109 (KS06), and evaluated whether the single nucleotide polymorphism (SNP) WUR10000125 (WUR) on chromosome 4 that was associated with viral load and weight gain under infection with NVSL also has an effect on response to infection across North American PRRSV isolates. Wood’s lactation curve was fitted to repeated viremia measurements to derive five curve characteristics that were evaluated.ResultsInfection with NVSL was characterized by reaching a 14 ± 2 % higher peak viremia (PV) 2.5 ± 0.6 days earlier (time to peak; TP) than KS06, followed by 36 ± 1 % faster virus clearance, which occurred 3.9 ± 0.7 days sooner. Weight gain from 0 to 42 days post-infection (WG) tended to be higher under infection with KS06 than NVSL (3.7 ± 1.5 kg). Estimates of heritability were moderate for both PRRSV isolates for viral load from 0 to 21 days post-infection (VL) (NVSL: 0.31 ± 0.06; KS06: 0.51 ± 0.09) and WG (NVSL: 0.33 ± 0.06; KS06: 0.31 ± 0.09). Strong negative genetic correlations were observed between VL and WG for both NVSL (−0.74 ± 0.10) and KS06 (−0.52 ± 0.17) infected pigs. Pigs with genotype AB at the WUR SNP had a more desirable phenotype than AA pigs for all traits under infection with NVSL, but only for VL and PV with KS06; effects on other traits were smaller and not significantly different from zero (P > 0.05). Genetic correlations of host response between isolates were strong for VL, WG and PV. Accounting for WUR genotype had little impact on these correlations, suggesting that response to PRRSV infection has a substantial polygenic component that is common between these two isolates.ConclusionsThese results suggest that the KS06 PRRSV isolate is less virulent than NVSL but that genetic selection for increased resistance to either of these genetically distinct isolates is expected to increase resistance to the other isolate.Electronic supplementary materialThe online version of this article (doi:10.1186/s12711-016-0222-0) contains supplementary material, which is available to authorized users.

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

“…However, KS06 resulted in a more persistent infection over time. The phenotypic correlation between VL and WG was small negative: −0.33 for NVSL and −0.23 for KS06 (Hess et al, 2016).…”

“…Genetics of the host was found to have little impact on whether or not a particular pig showed rebound, as the heritability of rebound was close to zero (0.03 ± 0.08) (Boddicker et al, 2012). The NVSL strain was found to be more virulent than KS06 because it reached higher peak viremia more rapidly and resulted in a 16% higher VL and 19% slower growth of the pigs (Hess et al, 2016). However, KS06 resulted in a more persistent infection over time.…”

“…Viremia after 21 dpi was characterized by 17 and 6% of pigs showing viremia rebound for NVSL and KS06 infections, respectively (Hess et al, 2016), characterized by statistical evidence of an increase in the level of serum viremia, following Islam et al (2013). This likely reflects escape of the PRRSV from the host's immune response.…”

“…Nevertheless, estimates of heritability were moderately high for both PRRSV isolates for VL (0.31 ± 0.06 for NVSL and 0.51 ± 0.09 for KS06) and for WG (NVSL: 0.33 ± 0.06 for NVSL and 0.31 ± 0.09 for KS06), indicating that 30-50% of the variation in host response of nursery pigs from the same cross following experimental PRRSV infection is due to differences in host genetics (Hess et al, 2016). Genetic correlations between VL and WG were substantial and negative for both NVSL (−0.74 ± 0.10) and KS06 (−0.52 ± 0.17), suggesting that genes that make pigs more resistant (lower VL) also tend to allow pigs to grow faster following PRRSV infection (Hess et al, 2016).…”

“…Genetic correlations between VL and WG were substantial and negative for both NVSL (−0.74 ± 0.10) and KS06 (−0.52 ± 0.17), suggesting that genes that make pigs more resistant (lower VL) also tend to allow pigs to grow faster following PRRSV infection (Hess et al, 2016).…”