Phenotypic effect of a single nucleotide polymorphism on SSC7 on fetal outcomes in PRRSV-2 infected gilts

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is one of the most common viral diseases affecting the global pork industry, causing significant economic loss in breeding herds and growing pigs. Control is challenging and genomic interventions can potentially yield alternative strategies to control PRRS virus (PRRSV) infection. We previously conducted a genome-wide association study to broaden our understanding of host genetics of fetal responses following maternal PRRSV infection and found that an intergenic single nucleotide polymorphism (SNP) near the DIO2 gene encoding the type II iodothyronine deiodinase, was significantly associated with fetal viability in response to maternal PRRSV infection. To determine the potential effect of this SNP on fetal outcomes including fetal viability, survival, growth and developmental characteristics in an independent pregnant gilt challenge model, we produced balanced homozygous fetal populations comprised of either the SNP's A or B allele. We assessed fetal viral loads in placenta, serum, and thymus, serum thyroid hormone levels, and growth and bone development by genotype at the SNP site. Unexpectedly, the BB genotype was not associated with greater odds ratio of fetal viability but was significantly related to reduced serum T4 level and increased area of the proximal humeral secondary ossification center (PHOC). To our knowledge, this is the first report of the variation in the genomic region influencing fetal T4 level and PHOC area in response to PRRSV infection. These results might implicate a functional effect of the genomic region on fetal thyroid hormone metabolism, which is partly involved in fetal bone biology during maternal PRRSV infection.