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This article is part of the supplement: Proceedings of the International Symposium on Animal Genomics for Animal Health (AGAH 2010)

Open Access Proceedings

Probing genetic control of swine responses to PRRSV infection: current progress of the PRRS host genetics consortium

Joan K Lunney1*, Juan Pedro Steibel2, James M Reecy3, Eric Fritz3, Max F Rothschild3, Maureen Kerrigan4, B Trible4 and Raymond RR Rowland4

Author affiliations

1 Animal Parasitic Diseases Laboratory, BARC, ARS, USDA, Beltsville, MD 20705, USA

2 Depts. Animal Science, and Fisheries and Wildlife, Michigan State Univ., East Lansing, MI 48824, USA

3 Dept. Animal Science, Center for Integrated Animal Genomics, Iowa State Univ., Ames, IA 50011, USA

4 Dept. Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State Univ., Manhattan, KS 66506, USA

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Citation and License

BMC Proceedings 2011, 5(Suppl 4):S30  doi:10.1186/1753-6561-5-S4-S30

Published: 3 June 2011

Abstract

Background

Understanding the role of host genetics in resistance to porcine reproductive and respiratory syndrome virus (PRRSV) infection, and the effects of PRRS on pig health and related growth, are goals of the PRRS Host Genetics Consortium (PHGC).

Methods

The project uses a nursery pig model to assess pig resistance/susceptibility to primary PRRSV infection. To date, 6 groups of 200 crossbred pigs from high health farms were donated by commercial sources. After acclimation, the pigs were infected with PRRSV in a biosecure facility and followed for 42 days post infection (dpi). Blood samples were collected at 0, 4, 7, 10, 14, 21, 28, 35 and 42 dpi for serum and whole blood RNA gene expression analyses; weekly weights were recorded for growth traits. All data have been entered into the PHGC relational database. Genomic DNAs from all PHGC1-6 pigs were prepared and genotyped with the Porcine SNP60 SNPchip.

Results

Results have affirmed that all challenged pigs become PRRSV infected with peak viremia being observed between 4-21 dpi. Multivariate statistical analyses of viral load and weight data have identified PHGC pigs in different virus/weight categories. Sera are now being compared for factors involved in recovery from infection, including speed of response and levels of immune cytokines. Genome-wide association studies (GWAS) are underway to identify genes and chromosomal locations that identify PRRS resistant/susceptible pigs and pigs able to maintain growth while infected with PRRSV.

Conclusions

Overall, the PHGC project will enable researchers to discover and verify important genotypes and phenotypes that predict resistance/susceptibility to PRRSV infection. The availability of PHGC samples provides a unique opportunity to continue to develop deeper phenotypes on every PRRSV infected pig.