P0607
Genetic Control of Swine Responses to PRRSV Infection: Progress of the PRRS Host Genetics Consortium

Date: Monday, January 14, 2013
Room: Grand Exhibit Hall
Joan Lunney , USDA, ARS, BARC, East Beltsville, MD
Igseo Choi , APDL, BARC, ARS, USDA, Beltsville, MD
Carlos J H Souza , USDA ARS BARC, Beltsville, MD
Karla PC Araujo , USDA ARS BARC, Beltsville, MD
Sam Abrams , USDA ARS BARC, Beltsville, MD
Juan P. Steibel , Department of Animal Science, Michigan State University, East Lansing, MI
Maria Arceo , Department of Animal Science, Michigan State University
Cathy Ernst , Department of Animal Science, Michigan State University, East Lansing, MI
James M. Reecy , Department of Animal Science, Iowa State University, Ames, IA
Eric Fritz , Iowa State University, Ames, IA
Jack Dekkers , Department of Animal Science, Iowa State University, Ames, IA
Nicholas Boddicker , Iowa State University, Ames, IA
Emily Waide , Department of Animal Science, Iowa State University, Ames, IA
Xia Zhao , Iowa State University, Ames, IA
Max F. Rothschild , Iowa State University, Ames, IA
Graham Plastow , University of Alberta, Edmonton, AB, Canada
Bob A Kemp , Genesus, Lethbridge, AB, Canada
John Harding , University of Saskatchewan, Saskatoon, SK, Canada
Maureen Kerrigan , Kansas State University
Benjmain R. Trible , Kansas State University
Raymond R. R. Rowland , Kansas State University
The most important infectious disease threatening pig production worldwide is porcine reproductive and respiratory syndrome (PRRS). The PRRS Host Genetics Consortium (PHGC) was established to probe the role of host genetics in resistance to PRRSV infection and related growth effects. Using a nursery pig model, 14 groups of 200 commercial crossbred pigs were infected with PRRS virus and followed for 42 days post infection (dpi). Blood serum and Tempus (RNA) samples were collected at 9 timepoints and weekly weights recorded. All pigs were viremic, peaking at 4-14 dpi. Genomic DNA was genotyped with the Porcine SNP60 SNPchip for genome wide association studies (GWAS) that identified a genomic region on swine chromosome 4 (SSC4) with significant impact on variation in viral load and growth response following viral challenge. Using Bayes-B analyses for 5 trials, 8 1-Mb regions accounted for 35.7% of the genetic variance for viral load from 0-21 dpi with an SSC4 region explaining 17.7%. For weight gain 10 regions accounted for 31.2% of the genetic variance with SSC4 accounting for 14.3%. Sera and RNA are now being analyzed using the Pigoligoarray, RNA-seq, QPCR and multiplex immunoassays to elucidate factors involved in viral replication, recovery from infection, including speed and levels of immune cytokine expression. These analyses and SSC4 region sequencing should identify markers that distinguish PRRS resistant/maximal growth pigs from PRRS susceptible/reduced growth pigs. PHGC funding: US National Pork Board, USDA ARS and NIFA, NRSP8 Swine Genome and Bioinformatics Coordinators, Genome Alberta/ALMA, Genome Canada, and private companies.