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

Abstract

<p>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 (<em>P</em> < 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 (<em>P</em> < 0.04) only for microscopic lung lesion scores but approached significance (<em>P</em> < 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.</p>