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Variation in host genetics influences PCVAD susceptibility

Wednesday, March 19, 2014: 10:00 AM
306-307 (Community Choice Credit Union Convention Center)
Taylor B. Engle , University of Nebraska-Lincoln, Lincoln, NE
Erin E. Jobman , University of Nebraska-Lincoln, Lincoln, NE
Tim W. Moural , University of Nebraska-Lincoln, Lincoln, NE
Autumn M. McKnite , University of Nebraska-Lincoln, Lincoln, NE
Sarah Y. Barnes , University of Nebraska-Lincoln, Lincoln, NE
Emily H. Davis , University of Nebraska-Lincoln, Lincoln, NE
Justin W. Bundy , University of Nebraska, Lincoln, NE
Theresa P. Johnson , University of Nebraska-Lincoln, Lincoln, NE
Jessica K. Qiu , University of Nebraska-Lincoln, Lincoln, NE
Judith A. Galeota , University of Nebraska-Lincoln, Lincoln, NE
Seth P. Harris , University of Nebraska-Lincoln, Lincoln, NE
Max F. Rothschild , Iowa State University, Ames, IA
Rodger K. Johnson , University of Nebraska - Lincoln, Lincoln, NE
Graham S. Plastow , University of Alberta, Edmonton, AB, Canada
Stephen D. Kachman , University of Nebraska - Lincoln, Lincoln, NE
Daniel C. Ciobanu , University of Nebraska, Lincoln, NE
Recorded Presentation (flv) Audio File
Abstract Text:

Porcine Circovirus type 2 (PCV2), the causative agent of Porcine Circovirus Associated Diseases (PCVAD), affects growth and can lead to mortality. Host genetics influences susceptibility and plays a role in PCVAD progression. The objective of this research was to identify major genetic variants and genes that influence immune response and PCVAD susceptibility. Various crossbred lines were experimentally infected with a PCV2b strain similar to a cluster of PCV2b strains known to induce clinical signs of PCVAD and high mortality. During a 28 d experimental challenge, weekly measurements of average daily gain (ADG), viremia, and PCV2 specific antibodies were profiled. Common sources of variation were evaluated by estimating pair-wise correlations between phenotypic and genomic prediction values and by genome-wide associations across traits. Viremia was the best indicator of decreased ADG following infection; moderate phenotypic correlations between viremia and ADG were observed starting with viremia at 14 d post infection (dpi) and ADG during the last two weeks of challenge (r = -0.31 to -0.39; P < 0.001).  The correlation between overall ADG (0 - 28 d) and viral load was -0.36. In contrast, the correlation between ADG and PCV2 specific antibodies, IgM (-0.12 to 0.05) and IgG (-0.02 to 0.11) were weak. Correlations between genomic prediction values were the largest between viremia at 21 dpi and ADG during the last 3 weeks of challenge (-0.27 to -0.33, P < 0.0001). A genome wide association study that included 56,433 SNPs uncovered two major SNPs that explain, 12.4% (ALGA0110477, SSC12) and 3.7% (ALGA0039682, SSC7, 29.3 Mb) respectively, of the genetic variation for viral load. The SNP ALGA0039682 is located next to the SLA II complex of genes known for their role in immune response. These SNPs partially explained the negative correlations between viremia and ADG. The genotype CC of ALGA0110477 was associated with lower viral load (58.6) compared to genotype TT (74.0, P < 0.0001) and genotype CT (67.3, P < 0.0001). Genotype CC was also associated with higher overall ADG (0.50 kg) compared to genotype TT (0.45 kg, P < 0.001) and genotype CT (0.47 kg, P < 0.05). These results could lead to increased knowledge of the swine immune system, and identification of genes involved in PCVAD susceptibility. Selection of parent stock based on DNA markers associated with PCVAD has the potential to reduce economic losses, improve animal welfare and provide alternatives to vaccination.

Keywords: Swine, PCVAD, Genetics

See more of: Breeding and Genetics II
See more of: Breeding and Genetics
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