Upregulation of interferon-alpha gene in bovine embryos produced in vitro in response to experimental infection with noncytophatic bovine-viral-diarrhea virus.

In-vitro fertilization is a routine livestock-breeding technique widely used around the world. Several studies have reported the interaction of bovine viral-diarrhea virus (BVDV) with gametes and in-vitro-produced (IVP) bovine embryos. Since, gene expression in BVDV-infected IVP bovine embryos is scarcely addressed. The aim of this work was to evaluate the differential expression of genes involved in immune and inflammatory response. Groups of 20-25 embryos on Day 6 (morula stage) were exposed (infected) or not (control) to an NCP-BVDV strain in SOF medium. After 24 h, embryos that reached expanded blastocyst stage were washed. Total RNA of each embryo group was extracted to determine the transcription levels of 9 specific transcripts related with antiviral and inflammatory response by SYBR Green real time quantitative (RT-qPCR). Culture media and an aliquot of the last embryos wash on Day 7 were analyzed by titration and virus isolation, respectively. A conventional PCR confirmed BVDV presence in IVP embryos. A significantly higher expression of interferon-α was observed in blastocysts exposed to NCP-BVDV compared to the controls (p < 0.05). In this study, the upregulation of INFα and TLR7 genes involved in inflammatory and immune response in BVDV-infected IVP bovine embryos is a new finding in this field. This differential expression suggest that embryonic cells could function in a manner like immune cells by recognizing and responding early to interaction with viral pathogens. These results provide new insights into the action of BVDV on the complex molecular pathways controlling bovine early embryonic development.

Diet effects on female reproduction in high growth (hg/hg) mice that are deficient in the Socs-2 gene.

The detrimental effect of larger body size on reproductive performance has been well documented in mouse models of overgrowth, such as Growth Hormone (GH) transgenics. This study describes the reproductive performance of the High Growth (HG) mouse model of overgrowth. The HG mouse model exhibits overgrowth due to a partially recessive autosomal mutation that increases growth rate and mature body size. The HG phenotype results from the lack of expression of Socs-2, which negatively regulates GH signaling. C57BL/6J (C57) and congenic C57BL/6J-hg/hg (HG) female mice were fed four diets differing in protein and energy content, starting at 8 weeks of age. A complete reproductive cycle from mating to weaning was evaluated. HG mice were 40% larger than C57 and had a higher feed intake throughout the experiment. Significant genotype x diet interactions were detected for growth, body composition and reproductive traits. HG females showed poor reproductive performance compared to controls as demonstrated by their lower fertility during mating, which was not overcome by changes in the diet. No differences were detected in litter size, but HG animals exhibited a longer gestation length and heavier pup weaning weights compared to controls. Reproductive impairment in HG seems to be the consequence of the lack of Socs-2 independent of the effects of increased body size on reproduction.