Expression data from porcine cells infected with TGEV wild-type (rTGEV-wt) or mutant (rTGEV-delta7) coronaviruses
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ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE41756 | GEO | 2013/09/30
SECONDARY ACCESSION(S): PRJNA178114
REPOSITORIES: GEO
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Project description:Innate immune response is the first line of antiviral defense resulting, in most cases, in pathogen clearance with minimal clinical consequences. Viruses have developed diverse strategies to evade innate immune response and to ensure their survival. Using transmissible gastroenteritis virus (TGEV) as a model, we previously reported that accessory gene 7 counteracts host antiviral response by its association with the catalytic subunit of protein phosphatase 1 (PP1c). A transcriptomic analysis was performed to further investigate the effect of gene 7 absence on the host cell. A recombinant TGEV virus lacking gene 7 expression (rTGEV-delta7) was previously generated in our laboratory. Porcine ST cells were mock infected or infected with wild type (rTGEV-wt) or mutant (rTGEV-delta7) virus. Gene expression was analyzed at 6 and 12 hours post infection (hpi) by using porcine Affymetrix microarray. Three biological replicates were made for each sample type.
2013-09-30 | E-GEOD-41756 | biostudies-arrayexpress
Project description:Transmissible gastroenteritis virus (TGEV; Coronaviridae family) causes huge economic losses to the swine industry. MicroRNAs (miRNAs) play a regulatory role in viral infection and may be involved in the mammalian immune response. Here, we report a comprehensive analysis of host miRNA expression in TGEV-infected swine testis (ST) cells. Deep sequencing generated 3,704,353 and 2,763,665 reads from uninfected ST cells and infected ST cells, respectively. The reads were aligned to known Sus scrofa pre-miRNAs in miRBase 19, identifying 284 annotated miRNAs. Certain miRNAs were differentially regulated during TGEV infection, which confirmed the hypothesis that specific miRNAs play a regulatory role in virus-host interactions. 59 unique miRNAs displayed significant differentially expression between the normal and TGEV-infected ST cell samples: 15 miRNAs were significantly up-regulated and 44 were significantly down-regulated. Stem-loop RT-PCR was carried out to determine the expression levels of specific miRNAs in the two samples, and the results were consistent with those of sequencing. Gene ontology enrichment analysis of host target genes demonstrated that the differentially expressed miRNAs are involved in regulatory networks, including cellular process, metabolic process, immune system process. This is the first report of the identification of ST cell miRNAs and the comprehensive analysis of the miRNA regulatory mechanism during TGEV infection, which revealed the miRNA molecular regulatory mechanisms for the viral infection, expression of viral genes and the expression of immune-related genes. The results presented here will aid research on the prevention and treatment of viral diseases. 2 ST(Porcine testicular cells) cell samples, ST: normal ST cell sample (contro sample), TGEV: TGEV (Transmissible gastroenteritis virus) infected ST cell samples
2015-01-08 | E-GEOD-64737 | biostudies-arrayexpress
Project description:Transmissible gastroenteritis virus (TGEV), a member of the coronaviridae family, could cause fatal diarrhea of piglets and result in numerous economic losses. Previous studies demonstrated that TGEV infection could lead to mitochondrial damage and up-regulate miR-4331 level. So miR-4331 may play an important regulatory role in the control of mitochondrial function. To explore the potential role of miR-4331 in mitochondrial damage, we adopted a strategy consisting of quantitative proteomic analysis of porcine kidney (PK-15) cells in response to miR-4331 and TGEV infection. Eventually, 69 differentially expressed proteins were gained. The target of miR-4331 was identified. The effects of miR-4331 and its target RB1 on mitochondrial Ca2+ level, mitochondrial membrane potential (MMP), interleukin-1 receptor accessory protein (IL1RAP), p38 MAPK signaling pathway were investigated. The results showed that miR-4331 elevated mitochondrial Ca2+ level, reduced MMP, targets Retinoblastoma 1 (RB1), up-regulated IL1RAP, and induced activation of p38 MAPK pathway during TGEV infection. RB1 was identified as the direct targets of miR-4331 and down-regulated IL1RAP, suppressed the activation of p38 MPAK, and attenuated TGEV-induced mitochondrial damage. In addition, IL1RAP played a positive role in activating p38 MAPK signaling and negative role in TGEV-induced mitochondrial damage. The data indicate that miR-4331 aggravates TGEV-induced mitochondrial damage by repressing expression of RB1, promoting IL1RAP, and activating p38 MAPK pathway.
2017-12-15 | PXD008174 | Pride
Project description:Transmissible gastroenteritis virus (TGEV; Coronaviridae family) causes huge economic losses to the swine industry. MicroRNAs (miRNAs) play a regulatory role in viral infection and may be involved in the mammalian immune response. Here, we report a comprehensive analysis of host miRNA expression in TGEV-infected swine testis (ST) cells. Deep sequencing generated 3,704,353 and 2,763,665 reads from uninfected ST cells and infected ST cells, respectively. The reads were aligned to known Sus scrofa pre-miRNAs in miRBase 19, identifying 284 annotated miRNAs. Certain miRNAs were differentially regulated during TGEV infection, which confirmed the hypothesis that specific miRNAs play a regulatory role in virus-host interactions. 59 unique miRNAs displayed significant differentially expression between the normal and TGEV-infected ST cell samples: 15 miRNAs were significantly up-regulated and 44 were significantly down-regulated. Stem-loop RT-PCR was carried out to determine the expression levels of specific miRNAs in the two samples, and the results were consistent with those of sequencing. Gene ontology enrichment analysis of host target genes demonstrated that the differentially expressed miRNAs are involved in regulatory networks, including cellular process, metabolic process, immune system process. This is the first report of the identification of ST cell miRNAs and the comprehensive analysis of the miRNA regulatory mechanism during TGEV infection, which revealed the miRNA molecular regulatory mechanisms for the viral infection, expression of viral genes and the expression of immune-related genes. The results presented here will aid research on the prevention and treatment of viral diseases.
2015-01-08 | GSE64737 | GEO
Project description:Emerging coronaviruses (CoVs) primarily cause severe gastroenteric or respiratory diseases in humans and animals, for which no approved therapeutics are available so far. Here A9, a receptor tyrosine kinase inhibitors (RTKIs) of the tyrphostin class was identified as a robust inhibitor of TGEV (Transmissible gastroenteritis virus) infection in cell-based assays. Time-of-addition studies suggested that A9 mainly acts at post-adsorption stage of the TGEV life cycle. Moreover, it also exhibited potent antiviral activity against various coronavirus replication, including MHV, PEDV and FIPV. We further investigated the mechanism of action of A9 against TGEV infection in vitro with comparative phosphoproteomics analysis. We specifically identified the A9 target, p38 and JNK1, the downstream molecules of receptor tyrosine kinases (RTKs) as required for efficient TGEV replication in vitro through plaque assay, qRT-PCR and western blotting assays. Additionally, tests of p38 and JNK1 inhibitors also indicated that interventions targeting p38 was more effective in suppressing TGEV propagation than the JNK. In conclusion, these findings indicate that the receptor tyrosine kinase inhibitor A9 can directly inhibits TGEV replication and its inhibitory activity on TGEV replication mainly regulated by targeting p38, which provide vital clues to design novel drugs against coronavirus.
2020-05-26 | PXD010685 | Pride
Project description:We designed a long-term culture system for porcine intestinal organoids from intestinal crypt or single Lgr5+ stem cells by combining previously defined insights in the growth requirements of intestinal epithelium of human and mouse. We showed that long-term cultured swine intestinal organoids were expanded in vitro more than six months at least and maintained the potential to differentiate into different types of cells. These organoids were successfully infected with porcine enteric coronavirus including porcine epidemic diarrhea virus (PEDV) and transmissible gastroenteritis virus (TGEV). RNA-seq analysis showed that robust induction of transcripts associated with antiviral signaling in response to enteric coronavrius infection, including a number of interferon-stimulated genes and cytokines. Moreover, gene set enrichment analysis indicated that PEDV infection could suppress immune response in organoids. This 3D intestinal organoid model offers a long-term, renewable resource for investigating porcine intestinal infections with a variety of pathogens.
2021-08-19 | GSE182240 | GEO
Project description:Transmissible gastroenteritis virus (TGEV) is a member of Coronaviridae family. Our previous research showed that TGEV infection could induce mitochondrial dysfunction and up-regulat miR-222 level. Therefore, we presumed that miR-222 might be implicated in regulating mitochondrial dysfunction induced by TGEV infection. To verify the hypothesis, the effect of miR-222 on mitochondrial dysfunction was detected and showed that miR-222 attenuated TGEV-induced mitochondrial dysfunction. To investigate the underlying molecular mechanism of miR-222 in TGEV-induced mitochondrial dysfunction, a quantitative proteomic analysis of PK-15 cells that were transfected with miR-222 mimics and infected with TGEV was performed. In total, 4151 proteins were quantified and 100 differentially expressed proteins were obtained (57 up-regulated, 43 down-regulated), among which thrombospondin-1 (THBS1) and cluster of differentiation 47 (CD47) were down-regulated. THBS1 was identified as the target of miR-222. Knockdown of THBS1 and CD47 increased mitochondrial Ca2+ level and decreased mitochondrial membrane potential (MMP) level. Together, our data establish a significant role of miR-222 in regulating mitochondrial dysfunction in response to TGEV infection.
2018-12-19 | PXD010927 | Pride
Project description:Innate responses to coronavirus are highly cell-specific and remain to date incompletely understood. Tissue-resident macrophages, which are infected by SARS-CoV2 in patients but inconsistently in vitro, exert critical but conflicting effects by secreting both anti-viral type I Interferons and tissue-damaging inflammatory cytokines. Steroids, the only class of host-targeting drugs approved for Covid19, indiscriminately suppress both responses, possibly impairing viral clearance. Here we set up in vitro culture systems with the prototypical murine coronavirus MHV that allow to separately investigate cell-intrinsic and -extrinsic proinflammatory and antiviral activities. We then studied the role of the lysine-demethylase LSD1, previously implicated in innate responses in cancer. We show that the NF-κB-dependent inflammatory response is selectively inhibited by ablating LSD1 with negligible impact on antiviral interferon response. LSD1 ablation additionally unleashed an interferon-independent antiviral response and blocked viral egress through the lysosomal pathway. A cell-intrinsic antiviral and anti-inflammatory activity of LSD1 inhibition was confirmed on in vitro and a recently developed aerosolized in vivo model of human SARS-COV2 infection. These results show that LSD1 controls innate responses against coronaviruses at multiple levels and provide a mechanistic rationale for repurposing LSD1 inhibitors, a class of drugs extensively studied in oncology, for Covid-19 treatment.
2023-06-24 | GSE169399 | GEO
Project description:Transmissible gastroenteritis virus (TGEV), a member of coronavirus, is the pathogen of TGE. We previously found 123 circular RNAs (circRNAs) were differential expression during activation of mitochondrial permeability transition in porcine intestinal epithelial cells-jejunum 2 cell line (IPEC-J2) in response to TGEV infection. Mitochondrial permeability transition pore (mPTP) is a transmembrane pore of mitochondria and plays a key role in MPT. mPTP abnormal opening causes MPT. Therefore, we postulated that circRNAs might be related to mPTP abnormal opening induced by TGEV. In this study, we found that circBIRC6-2 could inhibit the mPTP abnormal opening induced by TGEV. Interestingly, circBIRC6-2 encodes protein BIRC6-236aa. An open reading frame (ORF) and internal ribosomal entrance site (IRES) of circBIRC6-2 were identified. We also found that BIRC6-236aa rather than circBIRC6-2 inhibited the mPTP opening by overexpression of circBIRC6-2 related vectors. We obtained 91 proteins that interacted with BIRC6-236aa using immunoprecipitation-mass spectrometry (IP-MS). The interaction between voltage-dependent anion-selective channel protein 1 (VDAC1) and BIRC6-236aa was demonstrated through co-immunoprecipitation (Co-IP). Moreover, BIRC6-236aa could inhibit the formation of VDAC1 and Cyclophilin D (CypD) complexes. Overall, these results indicated that BIRC6-236aa antagonized mPTP opening by interacting with VDAC1 to weaken the extent of interaction between VDAC1 and CypD.
2022-10-13 | PXD029055 | Pride
Project description:Transmissible gastroenteritis virus
| PRJNA17139 | ENA