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Genetic analysis of reproductive traits and antibody response in a PRRS outbreak herd

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http://www.journalofanimalscience.org/content/early/recent
Original languageEnglish
Pages (from-to)2905-2921
JournalJournal of Animal Science
Volume92
Issue number7
Early online date30 May 2014
DOIs
Publication statusPublished - Jul 2014

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is the most economically significant disease impacting pig production in North America, Europe, and Asia, causing reproductive losses such as increased rates stillbirth and mummified piglets. The objective of this study was to explore the genetic basis of host response to the PRRS virus (PRRSV) in a commercial multiplier sow herd before and after a PRRS outbreak, using antibody response and reproductive traits. Reproductive data comprising number born alive (NBA), number alive at 24h (NA24), number stillborn (NSB), number born mummified (NBM), proportion born dead (PBD), number born dead (NBD), number weaned (NW), and number mortalities through weaning (MW) of 5,227 litters from 1,967 purebred Landrace sows, were used along with a pedigree comprising 2,995 pigs. The PRRS outbreak date was estimated from rolling averages of farrowing traits and used to split the data in a pre-PRRS phase and a PRRS phase. All 641 sows in the herd during the outbreak were blood sampled 46 days after the estimated outbreak date, and were tested for anti-PRRSV IgG using ELISA (sample-to-positive [S/P] ratio). Genetic parameters of traits were estimated separately for the pre-PRRS and PRRS phase data sets. Sows were genotyped using the PorcineSNP60 BeadChip, and genome-wide association studies (GWAS) were performed using method Bayes-B. Heritability estimates for reproductive traits ranged from 0.01 (NBM) to 0.12 (NSB), and from 0.01 (MW) to 0.12 (NBD) for the pre-PRRS and PRRS phases, respectively. S/P ratio had heritability (0.45) and strong genetic correlations with most traits, ranging from -0.72 (NBM) to 0.73 (NBA). In the pre-PRRS phase, regions associated with NSB and PBD explained 1.6% and 3% of the genetic variance, respectively. In the PRRS phase, regions associated with NBD, NSB, and S/P ratio explained 0.8%, 11%, and 50.6% of the genetic variance, respectively. For S/P ratio, two regions on SSC7 separated by 100 Mb explained 40% of the genetic variation, including a region encompassing the Major Histocompatibility Complex, which explained 25% of the genetic variance. These results indicate a significant genomic component associated with PRRSV antibody response and NSB in this dataset. Also, the high heritability and genetic correlation estimates for S/P ratio during the PRRS phase suggest that S/P ratio could be used as an indicator of the impact of PRRS on reproductive traits.

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