|Doeschl-Wilson, Andrea - SCOTTISH AGRICULTURAL COL|
|Kyriazakis, Ilias - UNIVERSITY OF THESSALY|
|Rothschild, Max - IOWA STATE UNIVERSITY|
|Galina-Pantoja, Lucina - PIC IMPROVEMENT COMPANY|
Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 30, 2009
Publication Date: May 1, 2009
Repository URL: http://jas.fass.org/cgi/content/abstract/jas.2008-1447v1
Citation: Doeschl-Wilson, A.B., Kyriazakis, I., Vincent, A., Rothschild, M.F., Thacker, E., Galina-Pantoja, L. 2009. Clinical and Pathological Responses of Pigs from Two Genetically Diverse Commercial Lines to Porcine Respiratory and Reproductive Syndrome Virus Infection. Journal of Animal Science. 87(5):1638-1647. Interpretive Summary: Porcine reproductive and respiratory syndrome virus (PRRSV) remains one of the most economically important disease agents in swine world wide. Previous studies have shown that lines or breeds of pigs are impacted at different levels by PRRSV infection. In this study, we investigated associations among disease and performance traits to try to understand biological responses to PRRSV infection. This study revealed significant line differences in growth during infection. The line of pigs with favorable growth traits tended to have less favorable outcomes in response to PRRSV infection. However, relationships between growth and disease traits varied with time, indicating that different disease related mechanisms operate at different times in the course of PRRSV infection. Therefore, the time of assessing host responses may influence the conclusions drawn about biological significance. This study also suggests that PRRSV related reductions in growth may be more strongly related to the duration of infection rather than the severity of infection.
Technical Abstract: The response to infection from porcine reproductive and respiratory syndrome virus (PRRSV) for two genetically diverse commercial pig lines was investigated. Seventy two pigs from each line, aged 6 weeks, were challenged with PRRSV VR-2385, and 66 littermates served as control. The clinical response to infection was monitored throughout the study and pigs were necropsized at 10 or 21 days post infection. Previous analyses showed significant line differences in susceptibility to PRRSV infection. This study revealed also significant line differences in growth during infection. Line B, characterized by a faster growth rate than Line A in the absence of infection, suffered more severe clinical disease and greater reduction in weight growth after infection. Correlations between growth and disease related traits were generally negative, albeit weak. Correlations were also weak amongst most clinical and pathological traits. Clinical disease traits such as respiratory scores and rectal temperatures were poor indicators for virus levels, pathological damage or growth during PRRSV infection. Relationships between traits varied over time, indicating that different disease related mechanisms may operate at different time scales and therefore that the time of assessing host responses may influence the conclusions drawn about biological significance. Three possible mechanisms underlying growth under PRRSV infection were proposed based on evidence from this and previous studies. It was concluded that a comprehensive framework describing the interaction between the biological mechanisms and the genetic influence on these would be desirable for achieving progress in the genetic control of this economically important disease.