An investigation of susceptibility to porcine reproductive and respiratory syndrome virus between two genetically diverse commercial lines of pigs

Abstract

The objective of this study was to determine whether host genetics play a role in susceptibility to the respiratory disease in growing pigs caused by the porcine reproductive and respiratory syndrome virus (PRRSV). Based on a previous study, 2 genetically diverse commercial lines of pigs that also were divergent in the susceptibility of monocyte-derived macrophages to PRRSV infection in vitro were selected for an in vivo challenge study. Based on the average percentage of infected macrophages for each line, a line derived from the Large White breed was characterized as fluorescence-activated cell sorting(hi) (FACS(hi)), and a line derived from Duroc and Pietrain breeds was characterized as FACS(lo). Pigs from each line were challenged at 6 wk of age with PRRSV VR-2385 and necropsied at 10 or 21 d after infection. Data collected included clinical evaluation of disease, virus titration in serum and lung lavage fluid, macroscopic lung lesion scores, and microscopic lung lesion scores. The FACS(lo) line had consistently more severe clinical disease compared with the FACS(hi) line in the early stages of infection. Differences between line means were significant (P < 0.05) at 10 d after infection for all variables just described, and the FACS(lo) line showed more severe signs of disease. By 21 d after infection, clinical signs and lesions were resolving, and the differences between lines were significant (P < 0.04) only for microscopic lung lesion scores but approached significance (P < 0.08) for virus titer in serum. At 21 d after infection, the relationship between the lines reversed; the FACS(hi) line had higher serum virus titers than the FACS(lo) line. This report provides evidence that strongly suggests the existence of a host genetic component in disease susceptibility to PRRSV and indicates that further study is warranted to define the cellular mechanisms that affect disease susceptibility.

Figure 1.

Daily least squares means of rectal temperatures by line. Line had a statistically significant effect over the trial period, P < 0.001. The fluorescence-activated cell sorting^hi (FACS^hi) line is represented by the solid line and diamond, and the FACS^lo line is represented by the dashed line and square.

Figure 2.

Log₁₀-transformed serum tissue culture titer in tissue culture infective dose₅₀ (TCID₅₀)/mL or quantitative competitive-reverse transcriptase-PCR (QC-RT-PCR) copy number per microliter at 10 d after infection. The least squares means ± SE for TCID₅₀/mL of serum virus titer at 10 d after infection were 10^{4.06 ± 0.05} for the fluorescence-activated cell sorting^hi (FACS^hi) line (solid black bar) and 10^{4.24 ± 0.05} for the FACS^lo line (solid white bar) over all 4 replicates, P < 0.02. Least squares means for copy number per microliter in serum QC-RT-PCR results for replicates 2, 3, and 4 at 10 d after infection were 10^{7.9 ± 0.09} for the FACS^hi line (hatched bar) and 10^{8.3 ± 0.07} for the FACS^lo line (solid gray bar), P < 0.003.

Figure 3.

Log₁₀-transformed serum tissue culture titer in tissue culture infective dose₅₀ (TCID₅₀)/mL or quantitative competitive-reverse transcriptase-PCR (QC-RT-PCR) copy number per microliter at 21 d after infection. The least squares means ± SE for TCID₅₀/mL serum virus titer were 10^{101.54 ± 0.28} for the fluorescence-activated cell sorting^hi (FACS^hi) line (solid black bar) and 10^{10.80 ± 0.28} for the FACS^lo line (solid white bar) over all 4 replicates, P < 0.08. Least squares means for copy number per microliter in serum QC-RT-PCR results for replicates 2, 3, and 4 at 21 d after infection were 10^{6.51 ± 0.50} for the FACS^hi line (hatched bar) and 10^{5.64 ± 0.50} for the FACS^lo line (solid gray bar), P < 0.24.