Porcine macrophages: ASFV-infected vs. mock-infected
Ontology highlight
ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE132905 | GEO | 2019/09/30
REPOSITORIES: GEO
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Project description:Porcine macrophages: ASFV-infected vs. mock-infected
| PRJNA549440 | ENA
Project description:African swine fever virus (ASFV) is one of the most devastating swine pathogens characterized by nearly 100% mortality in naive herds and was recently emerged the in China. In this study, we generated the expression profile of porcine alveolar macrophages (PAMs) infected with a high pathogenic ASFV (Pig/Heilongjiang/2018 (Pig/HLJ/18) ASFV). Our data indicated that ASFV infection lead to a strong inhibition of host immunity but promote chemokine-mediated signaling pathway and neutrophil chemotaxis. Moreover, ASFV infection can modulate the host miRNA involved regulation network, leading to a significant increase of host metabolism related genes and acceleration of virus replication. Furthermore, ASFV-derived viral small RNAs (vsRNAs) can target some host immune response related genes. In conclusion, our transcriptome-wide data provide some insights into the regulatory mechanism during ASFV infection.
2020-10-20 | GSE145954 | GEO
Project description:African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domesticated pigs that potentially is a worldwide economic threat. Using an expressed sequence tag (EST) library-based antisense method of random gene inactivation and a phenotypic screen for limitation of ASFV replication in cultured human cells, we identified six host genes whose cellular functions are required by ASFV. These included three loci, BAT3 (HLA-B-associated transcript 3), C1qTNF (C1q and tumor necrosis factor-related protein 6), and TOM40 (translocase of outer mitochondrial membrane 40), for which antisense expression from a tetracycline-regulated promoter resulted in reversible inhibition of ASFV production by >99%. The effects of antisense transcription of the BAT3 EST and also of expression in the sense orientation of this EST, which encodes amino acid residues 450 to 518 of the mature BAT3 protein, were investigated more extensively. Sense expression of the BAT3 peptide, which appears to reversibly interfere with BAT3 function by a dominant negative mechanism, resulted in decreased synthesis of viral DNA and proteins early after ASFV infection, altered transcription of apoptosis-related genes as determined by cDNA microarray analysis, and increased cellular sensitivity to staurosporine-induced apoptosis. Antisense transcription of BAT3 reduced ASFV production without affecting abundance of the virus macromolecules we assayed. Our results, which demonstrate the utility of EST-based functional screens for the detection of host genes exploited by pathogenic viruses, reveal a novel collection of cellular genes previously not known to be required for ASFV infection.
2006-12-10 | E-SMDB-3898 | biostudies-arrayexpress
Project description:African swine fever virus (ASFV) is the causative agent of African swine fever, a highly contagious and usually fatal disease in pigs. The pathogenesis of ASFV infection has not been clearly elucidated. Here, we used single-cell RNA-sequencing technology to survey the transcriptomic landscape of ASFV-infected primary porcine alveolar macrophages. The temporal dynamic analysis of viral genes revealed increased expression of viral transmembrane genes. Molecular characteristics in the ASFV-exposed cells exhibited the activation of antiviral signaling pathways with increased expression levels of interferon-stimulated genes and inflammatory- and cytokine-related genes. By comparing infected cells with unexposed cells, we showed that the unfolded protein response (UPR) pathway was activated in low viral load cells, while the expression level of UPR-related genes in high viral load cells was less than that in unexposed cells. Cells infected with various viral loads showed signature transcriptomic changes at the median progression of infection. Within the infected cells, differential expression analysis and coregulated virus–host analysis both demonstrated ASFV promoted metabolic pathways but inhibited interferon and UPR signaling, implying the regulation pathway of viral replication in host cells. Furthermore, our results revealed that the cell apoptosis pathway was activated upon ASFV infection. Mechanistically, the production of tumor necrosis factor alpha (TNF-α) induced by ASFV infection is necessary for cell apoptosis, highlighting the importance of TNF-α in ASFV pathogenesis. Collectively, the data provide insights into the comprehensive host responses and complex virus–host interactions during ASFV infection, which may instruct future research on antiviral strategies.
2022-04-05 | GSE168113 | GEO
Project description:African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domesticated pigs that potentially is a worldwide economic threat. Using an expressed sequence tag (EST) library-based antisense method of random gene inactivation and a phenotypic screen for limitation of ASFV replication in cultured human cells, we identified six host genes whose cellular functions are required by ASFV. These included three loci, BAT3 (HLA-B-associated transcript 3), C1qTNF (C1q and tumor necrosis factor-related protein 6), and TOM40 (translocase of outer mitochondrial membrane 40), for which antisense expression from a tetracycline-regulated promoter resulted in reversible inhibition of ASFV production by >99%. The effects of antisense transcription of the BAT3 EST and also of expression in the sense orientation of this EST, which encodes amino acid residues 450 to 518 of the mature BAT3 protein, were investigated more extensively. Sense expression of the BAT3 peptide, which appears to reversibly interfere with BAT3 function by a dominant negative mechanism, resulted in decreased synthesis of viral DNA and proteins early after ASFV infection, altered transcription of apoptosis-related genes as determined by cDNA microarray analysis, and increased cellular sensitivity to staurosporine-induced apoptosis. Antisense transcription of BAT3 reduced ASFV production without affecting abundance of the virus macromolecules we assayed. Our results, which demonstrate the utility of EST-based functional screens for the detection of host genes exploited by pathogenic viruses, reveal a novel collection of cellular genes previously not known to be required for ASFV infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2007-08-09 | E-GEOD-7581 | biostudies-arrayexpress
Project description:African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domesticated pigs that potentially is a worldwide economic threat. Using an expressed sequence tag (EST) library-based antisense method of random gene inactivation and a phenotypic screen for limitation of ASFV replication in cultured human cells, we identified six host genes whose cellular functions are required by ASFV. These included three loci, BAT3 (HLA-B-associated transcript 3), C1qTNF (C1q and tumor necrosis factor-related protein 6), and TOM40 (translocase of outer mitochondrial membrane 40), for which antisense expression from a tetracycline-regulated promoter resulted in reversible inhibition of ASFV production by >99%. The effects of antisense transcription of the BAT3 EST and also of expression in the sense orientation of this EST, which encodes amino acid residues 450 to 518 of the mature BAT3 protein, were investigated more extensively. Sense expression of the BAT3 peptide, which appears to reversibly interfere with BAT3 function by a dominant negative mechanism, resulted in decreased synthesis of viral DNA and proteins early after ASFV infection, altered transcription of apoptosis-related genes as determined by cDNA microarray analysis, and increased cellular sensitivity to staurosporine-induced apoptosis. Antisense transcription of BAT3 reduced ASFV production without affecting abundance of the virus macromolecules we assayed. Our results, which demonstrate the utility of EST-based functional screens for the detection of host genes exploited by pathogenic viruses, reveal a novel collection of cellular genes previously not known to be required for ASFV infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2007-08-09 | GSE7581 | GEO
Project description:Large DNA viruses are known to manipulate and modify host miRNAs during infection. Therefore the aim of this study was to investigate the impact of infection with the large DNA virus; African swine fever virus (ASFV) on host miRNAs. Small RNA sequencing libraries were prepared from RNA extracted from ASFV (Benin 97/1) infected primary porcine macrophages at 0, 6 and 16 hours post infection. Libraries were pooled and sequenced on 1 lane of an Illumina HiSeq, yielding sequences aligning to a total of 247 different mature Sus scrofa miRNAs. On average, 3779095 (± 1911525) miRNA reads were obtained per sample. The results revealed no widespread modification to host miRNAs, though a number of specific miRNAs were differentially expressed during ASFV infection. Notably, a small number of miRNAs (Ssc-miR-10b, Ssc-miR-144 and Ssc-miR-486) were rapidly upregulated 2-6 fold within the first hour of infection.
2020-07-28 | GSE115512 | GEO
Project description:We describe the transcriptomic recall response to African swine fever virus (ASFV) upon in vitro stimulation in porcine peripheral blood mononuclear cells (PBMC) obtained three weeks after receiving an intranasal dose of 106 pfu of the live attenuated BA71ΔCD2 vaccine prototype. PBMC from 4 unvaccinated and 4 vaccinated pigs were stimulated with BA71ΔCD2 or left untreated for 10 hours, RNA was extracted, and bulk RNA-sequencing was performed. Major transcriptional changes were found in BA71ΔCD2-stimulated samples from vaccinated pigs. Indeed, compared to unvaccinated control pigs, cells from vaccinated animals showed an upregulation of genes corresponding to a robust Th1 response. Together with this adaptive immune response, we also distinguished an innate immune response characterized by the expression of macrophage-related inflammatory genes. Altogether, our results demonstrate that intranasal vaccination of pigs with BA71ΔCD2 induce a systemic Th1 memory response that is concomitant with a rapid enhancement of innate immunity upon in vitro activation.
2022-10-24 | GSE196473 | GEO
Project description:Quantitiative analysis of proteomes of porcine macrophages and the stable cell line WSL infected with African swine fever virus using a nanoLC MALDI-Tof/Tof MS platform.
The impact of the infection on the two cell types was analyzed using Gene Ontology term and KEGG pathway enrichment analysis.
2021-10-26 | PXD028838 | JPOST Repository
Project description:African swine fever virus (ASFV) is a highly infectious and lethal swine pathogen that causes severe socio-economic consequences in affected countries. Unfortunately, effective vaccine for combating ASF is unavailable so far, and the prevention and control strategies for ASFV are still very limited. Toosendanin (TSN), a triterpenoid saponin extracted from the medicinal herb Melia toosendan Sieb. Et Zucc, has been demonstrated to possess analgesic, anti-inflammatory, anti-botulism and anti-microbial activities, and was used clinically as an anthelmintic, while the antiviral effect of TSN on ASFV has not been reported. In this study, we revealed that TSN exhibited a potent inhibitory effect on ASFV GD955-38 strain in porcine alveolar macrophages (PAMs) (EC50=0.085 μM, SI = 365) in a dose-dependent manner. TSN showed robust antiviral activity in different doses of ASFV infection and reduced the transcription and translation levels of ASFV p30 protein, viral genomic DNA quantity as well as viral titer at 24 and 48 hours post-infection. In addition, TSN did not affect virion attachment and release but intervened in its internalization in PAMs. Further investigations disclosed that TSN played its antiviral role by upregulating the host IFN-stimulated gene (ISG) IRF1 rather than by directly inactivating the virus particles. Overall, our results suggest that TSN is an effective antiviral agent against ASFV replication in vitro and may have the potential for clinical use.
2022-08-08 | GSE206118 | GEO