Clinical and pathological responses of pigs from two genetically diverse commercial lines to porcine reproductive and respiratory syndrome virus infection

• Published in: Journal of animal science Vol. 87; no. 5; pp. 1638 - 1647
• Main Authors: Doeschl-Wilson, A.B, Kyriazakis, I, Vincent, A, Rothschild, M.F, Thacker, E, Galina-Pantoja, L
• Format: Journal Article
• Language: English
• Published: Champaign, IL American Society of Animal Science 01.05.2009; Am Soc Animal Sci
• Subjects: Animal productions; Animals; Biological and medical sciences; body temperature; Body Weight; breathing; disease course; disease resistance; disease severity; Female; Fever; Fundamental and applied biological sciences. Psychology; genetic resistance; genetic variation; genotype; Least-Squares Analysis; liveweight gain; Male; Pneumonia - veterinary; porcine reproductive and respiratory syndrome; Porcine Reproductive and Respiratory Syndrome - genetics; Porcine Reproductive and Respiratory Syndrome - physiopathology; Porcine reproductive and respiratory syndrome virus; Porcine respiratory and reproductive syndrome virus - physiology; Random Allocation; Respiratory System - pathology; signs and symptoms (animals and humans); swine; Swine - genetics; Terrestrial animal productions; vertebrate viruses; Vertebrates; Farming animal; Respiratory disease; Arterivirus; Syndrome; porcine reproductive and respiratory syndrome; Pig; response to infection; Virus; Infection; Vertebrata; Meat animals; Mammalia; Arteriviridae; Swine infertility respiratory syndrome virus; Genetics; Artiodactyla; genetic susceptibility; Nidovirales; Ungulata
• ISSN: 0021-8812; 1525-3163
• DOI: 10.2527/jas.2008-1447

The response to infection from porcine reproductive and respiratory syndrome virus (PRRSV) for 2 genetically diverse commercial pig lines was investigated. Seventy-two pigs from each line, aged 6 wk, were challenged with PRRSV VR-2385, and 66 litter-mates served as control. The clinical response to infection was monitored throughout the study and pigs were necropsied at 10 or 21 d postinfection. Previous analyses showed significant line differences in susceptibility to PRRSV infection. This study also revealed significant line differences in growth during infection. Line B, characterized by faster growth rate than line A in the absence of infection, suffered more severe clinical disease and greater reduction in BW growth after infection. Correlations between growth and disease-related traits were generally negative, albeit weak. Correlations were also weak among most clinical and pathological traits. Clinical disease traits such as respiratory scores and rectal temperatures were poor indicators of 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.