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Journal of Animal Science Abstract - Quantitative Genetics

Clinical and pathological responses of pigs from two genetically diverse commercial lines to porcine reproductive and respiratory syndrome virus infection1


This article in

  1. Vol. 87 No. 5, p. 1638-1647
    Received: Sept 01, 2008
    Accepted: Jan 16, 2009
    Published: December 5, 2014

    2 Corresponding author(s):

  1. A. B. Doeschl-Wilson*2,
  2. I. Kyriazakis,
  3. A. Vincent,
  4. M. F. Rothschild§,
  5. E. Thacker and
  6. L. Galina-Pantoja#
  1. Scottish Agricultural College, Sustainable Livestock Systems, King’s Buildings, West-Mains Road Edinburgh, EH9 3JG, United Kingdom;
    Faculty of Veterinary Medicine, University of Thessaly, Trikalon 224, GR-43100, Karditsa, Greece;
    Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames 50011;
    Department of Animal Science, Center for Integrated Animal Genomics, Iowa State University, Ames 50011; and
    Pig Improvement Company, 100 Bluegrass Commons Blvd., Hendersonville, TN 37075


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.

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