TY - JOUR
T1 - Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs
AU - Dekkers, Jack
AU - Rowland, Raymond R.R.
AU - Lunney, Joan K.
AU - Plastow, Graham
N1 - Funding Information:
The projects described in this paper are supported by National Pork Board grants, USDA NIFA (awards 2008-55620-19132 , 2010-65205-20433 and 2013-68004-20362 ), Genome Canada , Genome Alberta and the Alberta Livestock and Meat Agency , PigGen Canada , Canadian Swine Breeders Association , Canadian Centre for Swine Improvement , the NRSP-8 Swine Genome and Bioinformatics Coordination projects , and the PRRS Host Genetics Consortium consisting of USDA ARS , Kansas State University , Iowa State University , Michigan State University , Washington State University , Purdue University , University of Nebraska-Lincoln , University of Saskatchewan , University of Alberta , PIC/Genus , Choice Genetics , Fast Genetics , Genesus, Inc. , TOPIGS , PigGen Canada, Inc. , IDEXX Laboratories , and Tetracore, Inc .
Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2017/9
Y1 - 2017/9
N2 - PRRS is the most costly disease in the US pig industry. While vaccination, biosecurity and eradication effort have had some success, the variability and infectiousness of PRRS virus strains have hampered the effectiveness of these measures. We propose the use of genetic selection of pigs as an additional and complementary effort. Several studies have shown that host response to PRRS infection has a sizeable genetic component and recent advances in genomics provide opportunities to capitalize on these genetic differences and improve our understanding of host response to PRRS. While work is also ongoing to understand the genetic basis of host response to reproductive PRRS, the focus of this review is on research conducted on host response to PRRS in the nursery and grow-finish phase as part of the PRRS Host Genetics Consortium. Using experimental infection of large numbers of commercial nursery pigs, combined with deep phenotyping and genomics, this research has identified a major gene that is associated with host response to PRRS. Further functional genomics work identified the GBP5 gene as harboring the putative causative mutation. GBP5 is associated with innate immune response. Subsequent work has validated the effect of this genomic region on host response to a second PRRSV strain and to PRRS vaccination and co-infection of nursery pigs with PRRSV and PCV2b. A genetic marker near GBP5 is available to the industry for use in selection. Genetic differences in host response beyond GBP5 appear to be highly polygenic, i.e. controlled by many genes across the genome, each with a small effect. Such effects can by capitalized on in a selection program using genomic prediction on large numbers of genetic markers across the genome. Additional work has also identified the genetic basis of antibody response to PRRS, which could lead to the use of vaccine response as an indicator trait to select for host response to PRRS. Other genomic analyses, including gene expression analyses, have identified genes and modules of genes that are associated with differences in host response to PRRS and can be used to further understand and utilize differences in host response. Together, these results demonstrate that genetic selection can be an additional and complementary tool to combat PRRS in the swine industry.
AB - PRRS is the most costly disease in the US pig industry. While vaccination, biosecurity and eradication effort have had some success, the variability and infectiousness of PRRS virus strains have hampered the effectiveness of these measures. We propose the use of genetic selection of pigs as an additional and complementary effort. Several studies have shown that host response to PRRS infection has a sizeable genetic component and recent advances in genomics provide opportunities to capitalize on these genetic differences and improve our understanding of host response to PRRS. While work is also ongoing to understand the genetic basis of host response to reproductive PRRS, the focus of this review is on research conducted on host response to PRRS in the nursery and grow-finish phase as part of the PRRS Host Genetics Consortium. Using experimental infection of large numbers of commercial nursery pigs, combined with deep phenotyping and genomics, this research has identified a major gene that is associated with host response to PRRS. Further functional genomics work identified the GBP5 gene as harboring the putative causative mutation. GBP5 is associated with innate immune response. Subsequent work has validated the effect of this genomic region on host response to a second PRRSV strain and to PRRS vaccination and co-infection of nursery pigs with PRRSV and PCV2b. A genetic marker near GBP5 is available to the industry for use in selection. Genetic differences in host response beyond GBP5 appear to be highly polygenic, i.e. controlled by many genes across the genome, each with a small effect. Such effects can by capitalized on in a selection program using genomic prediction on large numbers of genetic markers across the genome. Additional work has also identified the genetic basis of antibody response to PRRS, which could lead to the use of vaccine response as an indicator trait to select for host response to PRRS. Other genomic analyses, including gene expression analyses, have identified genes and modules of genes that are associated with differences in host response to PRRS and can be used to further understand and utilize differences in host response. Together, these results demonstrate that genetic selection can be an additional and complementary tool to combat PRRS in the swine industry.
KW - Host Genetics
KW - Pigs
KW - PRRS
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U2 - 10.1016/j.vetmic.2017.03.026
DO - 10.1016/j.vetmic.2017.03.026
M3 - Review article
C2 - 28385270
AN - SCOPUS:85016549907
SN - 0378-1135
VL - 209
SP - 107
EP - 113
JO - Veterinary Microbiology
JF - Veterinary Microbiology
ER -