Transcriptome analysis of MDBK cells infected with non-cytopathic field strains of bovine viral diarrhea virus (BVDV)
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ABSTRACT:
ORGANISM(S): Bos taurus
PROVIDER: GSE166528 | GEO | 2021/02/11
REPOSITORIES: GEO
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Project description:Transcriptional profiling by array was performed to investigate differentially expressed genes (DEGs) in BVDV-infected MDBK cells and to further explore the molecular mechanism of underlying functional changes caused by infection.
2021-02-07 | GSE166288 | GEO
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
2014-12-16 | E-GEOD-61251 | biostudies-arrayexpress
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).
2014-12-16 | GSE61251 | GEO
Project description:Transcriptome analysis of MDBK cells infected with non-cytopathic field strains of bovine viral diarrhea virus (BVDV)
| PRJNA701229 | ENA
Project description:Transcriptome analysis of MDBK cells infected with cytopathic bovine viral diarrhea virus (BVDV)
| PRJNA700064 | ENA
Project description:Endoplasmic reticulum (ER) stress signaling is an adaptive cellular response to the loss of ER Ca(2+) homeostasis and/or the accumulation of misfolded, unassembled, or aggregated proteins in the ER lumen. ER stress-activated signaling pathways regulate protein synthesis initiation and can also trigger apoptosis through the ER-associated caspase 12. Viruses that utilize the host cell ER as an integral part of their life cycle would be predicted to cause some level of ER stress. Bovine viral diarrhea virus (BVDV) is a positive-stranded RNA virus of the Flaviviridae family. BVDV and related flaviviruses use the host ER as the primary site of envelope glycoprotein biogenesis, genomic replication, and particle assembly. We are using a cytopathic strain of BVDV (cpBVDV) that causes cellular apoptosis as a model system to determine how virus-induced ER stress contributes to pathogenesis. We show that, in a natural infection of MDBK cells, cpBVDV activates the ER transmembrane kinase PERK (PKR-like ER kinase) and causes hyperphosphorylation of the translation initiation factor eIF2 alpha, consistent with the induction of an ER stress response. Additionally, we show that initiation of cellular apoptosis correlates with downregulation of the antiapoptotic Bcl-2 protein, induced expression of caspase 12, and a decrease in intracellular glutathione levels. Defining the molecular stress pathways leading to cpBVDV-induced apoptosis provides the basis to study how other ER-tropic viruses, such as hepatitis C and B viruses, modulate the host cell ER stress response during the course of persistent infection.
| S-EPMC136515 | biostudies-literature
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.
2024-05-29 | GSE255721 | GEO
Project description:Bovine viral diarrhea virus (BVDV), a Flaviviridae pestivirus, is arguably one of the most widespread cattle pathogens worldwide. Each of its two genotypes has two biotypes, non-cytopathic (ncp) and cytopathic (cp). Only the ncp biotype of BVDV may establish persistent infection in the fetus when infecting a dam early in gestation, a time point which predates maturity of the adaptive immune system. Such fetuses may develop and be born healthy but remain infected for life. Due to this early initiation of fetal infection and to the expression of interferon antagonistic proteins, persistently infected (PI) animals remain immunotolerant to the infecting viral strain. Although only accounting for some 1% of all animals in regions where BVDV is endemic, PI animals ensure the viral persistence in the host population. These animals may, however, develop the fatal mucosal disease, which is characterized by widespread lesions in the gastrointestinal tract. Cp BVD virus, in addition to the persisting ncp biotype, can be isolated from such animals. The cp viruses are characterized by unrestrained genome replication, and their emergence from the persisting ncp ones is due to mutations that are unique in each virus analyzed. They include recombinations with host cell mRNA, gene translocations and duplications, and point mutations. Cytopathic BVD viruses fail to establish chains of infection and are unable to cause persistent infection. Hence, these viruses illustrate a case of "viral emergence to extinction" - irrelevant for BVDV evolution, but fatal for the PI host.
| S-EPMC2850149 | biostudies-literature
Project description:Infections with bovine viral diarrhea virus (BVDV) contribute significantly to health-related economic losses in the beef and dairy industries and are widespread throughout the world. Severe acute BVDV infection is characterized by a gastrointestinal (GI) inflammatory response. The mechanism of inflammatory lesions caused by BVDV remains unknown. The interstitial cells of Cajal (ICC) network plays a pivotal role as a pacemaker in the generation of electrical slow waves for GI motility, and it is crucial for the reception of regulatory inputs from the enteric nervous system. The present study investigated whether ICC were a good model for studying GI inflammatory lesions caused by BVDV infection. Primary ICC were isolated from the duodenum of Merino sheep. The presence of BVDV was detected in ICC grown for five passages after BVDV infection, indicating that BVDV successfully replicated in ICC. After infection with BVDV strain TC, the cell proliferation proceeded slowly or declined. Morphological changes, including swelling, dissolution, and formation of vacuoles, of ICC were observed, pointing to quantitative, morphological and functional changes of ICC. Therefore, RNA sequencing (RNA-Seq) was performed to investigate differentially expressed genes (DEGs) in BVDV-infected ICC and to further explore the molecular mechanism of underlying quantitative, morphological and functional changes of ICC. Eight hundred six genes were differentially expressed upon BVDV infection, of which 538 genes were upregulated and 268 genes were downregulated. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the 806 DEGs were significantly enriched in 27 pathways, including cytokine-cytokine receptor interaction, interleukin (IL)-17 signaling, mitogen-activated protein kinase (MAPK) signaling pathway. Finally, 21 DEGs were randomly selected, and the relative repression levels of these genes were tested using the quantitative real-time PCR (qRT-PCR) to validate the RNA-Seq results. The results showed that the related expression levels of 21 DEGs were similar to RNA-Seq. This study is the first to establish a new infection model for investigating GI inflammatory lesions induced by BVDV infection.
2019-06-01 | GSE122344 | GEO
Project description:BackgroundBovine Viral Diarrhea Virus (BVDV) infection is widespread in cattle worldwide, causing important economic losses. Pathogenesis of the disease caused by BVDV is complex, as each BVDV strain has two biotypes: non-cytopathic (ncp) and cytopathic (cp). BVDV can cause a persistent latent infection and immune suppression if animals are infected with an ncp biotype during early gestation, followed by a subsequent infection of the cp biotype. The molecular mechanisms that underscore the complex disease etiology leading to immune suppression in cattle caused by BVDV are not well understood.ResultsUsing proteomics, we evaluated the effect of cp and ncp BVDV infection of bovine monocytes to determine their role in viral immune suppression and uncontrolled inflammation. Proteins were isolated by differential detergent fractionation and identified by 2D-LC ESI MS/MS. We identified 137 and 228 significantly altered bovine proteins due to ncp and cp BVDV infection, respectively. Functional analysis of these proteins using the Gene Ontology (GO) showed multiple under- and over- represented GO functions in molecular function, biological process and cellular component between the two BVDV biotypes. Analysis of the top immunological pathways affected by BVDV infection revealed that pathways representing macropinocytosis signalling, virus entry via endocytic pathway, integrin signalling and primary immunodeficiency signalling were identified only in ncp BVDV-infected monocytes. In contrast, pathways like actin cytoskeleton signalling, RhoA signalling, clathrin-mediated endocytosis signalling and interferon signalling were identified only in cp BDVD-infected cells. Of the six common pathways involved in cp and ncp BVDV infection, acute phase response signalling was the most significant for both BVDV biotypes. Although, most shared altered host proteins between both BVDV biotypes showed the same type of change, integrin alpha 2b (ITGA2B) and integrin beta 3 (ITGB3) were down- regulated by ncp BVDV and up- regulated by cp BVDV infection.ConclusionsThis study shows that, as we expected, there are significant functional differences in the host proteins that respond to cp or ncp BVDV infection. The combined use of GO and systems biology network modelling facilitated a better understanding of host-pathogen interactions.
| S-EPMC3026383 | biostudies-literature