P0371
Validation of Genetic Makers for Pig Resistance to PRRSV Infection

Date: Monday, January 12, 2015
Room:
Pengxia Niu , Chungbuk National University, Cheongju, South Korea
Nadeen Shabir , Chonbuk National University/College of Veterinary Medicine, Jeonju, South Korea
Amina Khatun , Chonbuk National University/College of Veterinary Medicine, Jeonju, South Korea
Suna Gu , Chonbuk National University/Division of Biotechnology, Jeonju, South Korea
Kwan-Suk Kim , Chungbuk National University, Chungcheongbuk, South Korea
Sang-Myoung Lee , Chonbuk National University/Division of Biotechnology, Jeonju, South Korea
Won-Il Kim , Chonbuk National University, Jeonju, South Korea
Porcine reproductive and respiratory syndrome (PRRS) caused by PRRS virus (PRRSV) is the economically most important disease to the swine industry.  Previous study suggested a few of candidate genes on the swine defense to PRRSV, such as interferon stimulated guanylate-binding protein family genes, and PRRSV receptor genes.  Here, to validate and better understand the host immune response to PRRSV at genetic level, we investigated the effects of variations in porcine GBP1, MX1 and CD163 genes on host growth and immune response to PRRSV infection in an experimental condition. In this study, our results showed that viremia negatively affected growth rate as expected (r = -0.599); GBP1-AG pigs have significantly higher growth rate during 11-25 days post infection (DPI) and lower viremia at 11 and 18 DPI as well as higher CD4+ and CD8+CD25+ cells; CD163-CC pigs had a significantly lower viremia at 18 DPI; and MX1-Dd had significantly higher CD4+ cells. Taken together, these results suggested the GBP1 polymorphism was the most effective marker among those three markers. A higher resistance of GBP1-AG animal to PRRS might be a consequence of increasing activation of CD8+ and CD4+ T cells of the infected animals.