Project description:Non-canonical microRNAs (miRNAs) are a class of short endogenous RNA molecules with the ability to control development, autophagy, apoptosis and the stress response in eukaryotes by pairing with partially complementary sites in the 3' untranslated regions (UTRs) of targeted genes. Recent studies have demonstrated that miRNAs serve as critical effectors in intricate networks of host-pathogen interactions. Thereforce, the differential expression of miRNAs were evaluated in Madin-Darby bovine kidney (MDBK) cells infected with bovine viral diarrhea virus (BVDV) NADL (100 TCID50/ 0.1 ml) for 6 h compared to normal MDBK cells using Solexa high-throughput sequencing technology (BGI, China). Examination of small RNA populations in BVDV infected MDBK cells compared to MDBK cells
Project description:Non-canonical microRNAs (miRNAs) are a class of short endogenous RNA molecules with the ability to control development, autophagy, apoptosis and the stress response in eukaryotes by pairing with partially complementary sites in the 3' untranslated regions (UTRs) of targeted genes. Recent studies have demonstrated that miRNAs serve as critical effectors in intricate networks of host-pathogen interactions. Thereforce, the differential expression of miRNAs were evaluated in Madin-Darby bovine kidney (MDBK) cells infected with bovine viral diarrhea virus (BVDV) NADL (100 TCID50/ 0.1 ml) for 6 h compared to normal MDBK cells using Solexa high-throughput sequencing technology (BGI, China).
Project description:Bovine Viral Diarrhea Virus (BVDV) is an endemic virus of North American cattle populations with significant economic and animal health impacts. While BVDV infection has a myriad of clinical manifestations, a unique and problematic outcome is the establishment of a persistently infected (PI) animal following in-utero viral infection. While it is well established that PI animals serve as a constant reservoir of BVDV, the mechanism for the maintained infection remains unknown despite multiple theories. The purpose of this study was to use transcriptome analysis to further define long term immune status of adult PI cattle and offer insight into the potential mechanistic establishment of persistent BVDV infection, in utero. Peripheral blood mononuclear cells were collected from PI beef cattle (N=6) and uninfected controls (N=6) for targeted RNAseq analysis conducted using 54 genes of interest and followed by pathway enrichment analysis. Analysis revealed 29 differentially expressed genes (FDR < 0.05, fold change > 2) representing 14 significant KEGG pathways between PI and control animals (FDR < 0.05). Transcriptome changes indicate chronic upregulation of interferon gamma (IFNG) with unexpected expression of related genes, suggesting a maintained stimulation of the PI immune system resulting in virus-mediated dysregulation of immune function.
Project description:The impact of late-term fetal bovine viral diarrhea virus (BVDV) transient infections (TI) on fetal growth and methylome was examined by inoculating pregnant heifers with a noncytopathic (ncp) type 2 BVDV suspended in media or media alone (sham-inoculated controls) on day 175 of gestation to generate TI (n=11) and control heifer calves (n=12). Blood samples were collected at birth. White blood cells (WBC) were separated for DNA extraction. Fetal infection in calves was confirmed by positive virus serum neutralizing antibody titers at birth and control calves were seronegative. Both control and TI calves were negative for BVDV RNA in WBCs by RT-PCR. DNA methyl seq analysis of WBC DNA demonstrated 2,349 differentially methylated cytosines (p≤0.05) including 1,277 hypomethylated cytosines, 1.072 hypermethylated cytosines, 84 differentially methylated regions based on CpGs in promoters and 89 DMRs based on CpGs in exons of TI WBC DNA compared to controls. Fetal BVDV infection during late gestation resulted in epigenomic modifications predicted to affect fetal and organ development pathways suggesting potential consequences for postnatal growth and health of TI cattle.
