Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/4/2005
Publication Date: 1/1/2006
Citation: Vincent, A.L., Thacker, B.J., Halbur, P.G., Rothschild, M.F., Thacker, E.L. 2006. An investigation of susceptibility to porcine reproductive and respiratory syndrome virus between two genetically diverse commercial lines of pigs. Journal of Animal Science. 84(1):49-57. Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is considered the most important disease to the swine industry worldwide. Measures to control PRRS virus have been largely unsuccessful, making selection of pigs with increased resistance to this pathogen highly attractive. We evaluated disease parameters in two lines of pigs from a commercial breeding herd selected for study based on a laboratory screening assay using whole blood. This study demonstrates that genetic variation in susceptibility to PRRSV appears to exist in cross-bred commercial pig populations and further study is warranted to investigate selection strategies to increase resistance to this important pathogen.
Technical Abstract: The objective of this study was to determine if host genetics plays 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, two genetically diverse commercial lines of pigs that were also divergent in the susceptibility of monocyte derived macrophages to PRRSV infection in vitro were selected for an in vivo challenge study. A line derived from the Large White breed was characterized as FACS**hi and a line derived from Duroc and Pietrain breeds was characterized as FACS**lo, based on each line’s average percentage of infected macrophages. Pigs from each line were challenged at 6 wk of age with PRRSV VR-2385 and necropsied at 10 or 21 days post infection (DPI). 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 to the FACS**hi line in the early stages of infection. Differences between line means were statistically significant at 10 DPI for all variables described above, with the FACS**lo line showing more severe signs of disease. By 21 DPI, clinical signs and lesions were resolving and the differences between lines were statistically significant only for microscopic lung lesion scores, but was approaching significance for virus titer in serum. At 21 DPI the relationship between the lines reversed with the FACS**hi line having higher serum virus titers. This report provides evidence that strongly suggests the existence of a host genetic component in disease susceptibility to PRRS, and indicates that further study is warranted to define the cellular mechanisms that affect disease susceptibility.