|Hay, El Hamidi|
|XU, LINGYANG - Chinese Academy Of Agricultural Sciences|
|ZHOU, YANG - Northwest Agricultural & Forestry University|
|ROWLAND, ROBERT - Kansas State University|
|Liu, Ge - George|
Submitted to: Journal of Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/14/2016
Publication Date: 5/24/2017
Citation: Hay, E.A., Choi, I., Xu, L., Zhou, Y., Rowland, R., Lunney, J.K., Liu, G. 2017. CNV analysis of host responses to porcine reproductive and respiratory syndrome virus infection. Journal of Genomics. 5:58-63.
Interpretive Summary: PRRS currently is the most economically significant disease to affect US swine production. Using high-density SNP array, we studied copy number variations associated with the host response to PRRS virus infection. We found several candidate genes in these CNV regions, which were involved in immune response pathways. Farmers, scientist, and policy planners who need improve animal health and production based on genome-enable animal selection will benefit from this study.
Technical Abstract: Porcine reproductive and respiratory syndrome (PRRS) is a devastating disease with a significant impact on the swine industry causing major economic losses. Recent studies revealed a region on Sus Scrofa chromosome (SSC) 4 associated with serum viremia and weight gain in pigs infected with the PRRS virus. The objective of this study is to examine copy number variations (CNVs) associated with the host response to PRRS virus infection. Copy number variations have been reported to affect various phenotypes. In this study, genome wide CNV analysis was performed using 1,324 animals genotyped with SNP60 BeadChip. After quality control, a total of 7097 CNVs and 271 CNV regions with varying sizes were discovered. The two phenotypes related to host response to the virus used in this study are viral load (VL, area under the curve of log-transformed serum viremia from 0 to 21 days post infection) and weight gain (WG42 from 0 to 42 days post infection). To investigate potential effects of CNVs on host response to PRRS, groups of animals with extreme high and low estimated breeding values (EBVs) for both traits were generated. For viral load, the two groups are referred to as virus resistant (100_R) for animals with low EBVs and susceptible (100_S) for animals with high EBVs. For WG42, the two groups are simply referred to as high and low depending on their EBVs. For viral load, 163 CNV regions were identified with a total length of 84 Mb from 100_S group of animals and 159 CNV regions with a total length of 76 Mb from 100_R group. For the second trait, WG42, 156 (79 Mb) and 126 (68 Mb) CNV regions were detected for low and high groups, respectively. Several genes were found in these CNV regions and network analyses revealed association of these genes with molecules regulating in immune response pathways.