ASFV-G-∆I177L
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ABSTRACT:
PROVIDER: PRJEB84951 | ENA |
REPOSITORIES: ENA
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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.
2006-12-10 | E-SMDB-3898 | biostudies-arrayexpress
Project description:African swine fever virus (ASFV) is a large, icosahedral, double-stranded DNA virus in the Asfarviridae family and the causative agent of African swine fever (ASF). ASFV causes a hemorrhagic fever with high mortality rates in domestic and wild pigs. ASFV contains an open reading frame named EP152R, previous research has shown that EP152R is an essential gene for virusrescue in swine macrophages. However, the detailed functions of ASFV EP152R remain elusive. Herein, we demonstrate that EP152R, a membrane protein located in the endoplasmic reticulum (ER), induces ER stress and swelling, triggering the PERK/eIF2α pathway and broadly inhibiting host protein synthesis in vitro. Additionally, EP152R strongly promotes immune evasion, reduces cell proliferation, and alters cellular metabolism. These results suggest that ASFV EP152R plays a critical role in the intracellular environment, facilitating viral replication. Furthermore, virus-level experiments have shown that the knockdown of EP152R or PERK inhibitors efficiently affects viral replication by decreasing viral gene expression. In summary, these findings reveal a series of novel functions of ASFV EP152R and have important implications for understanding host-pathogen interactions.
2024-08-22 | GSE275101 | 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. Keywords: Logical Set
2007-08-09 | GSE7581 | GEO
Project description:African swine fever virus (ASFV) is a highly contagious pathogen that primarily affects domestic and wild pigs with specific tropism to porcine alveolar macrophages (PAMs). However, the host receptors involved in ASFV infection remain unknow. Here, we present a multi-omic epigenetic atlas of ASFV-exposed PAMs and profile 3D chromatin architecture and single-nucleus chromatin accessibility landscapes (sn-ATAC)
2025-04-18 | GSE231435 | GEO
Project description:Transcriptional profiling of porcine macrophages infected with Afraican swine fever virus (ASFV) infected cells and mock infection was conducted in this experiment.
2019-09-30 | GSE132905 | 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:In this project we would like to study immune responses to African swine fever virus in pigs. We have realized a large animal experiment using two different viruses and pigs with different immune status. We have collected paxgene blood RNA tubes in order to investigate transcriptional changes at different stages of the early immune response.
2022-07-06 | E-MTAB-11634 | biostudies-arrayexpress
Project description:The NF-κB pathway is an essential signaling cascade in the defence against viral infections, including African swine fever virus (ASFV) infection. ASFV encodes more than 151 proteins via its own transcription machinery and possesses a great capacity to evade or subvert antiviral innate immune responses. Although some of these viral proteins have been reported, many remain unknown. In this study，we find pH108R, an inner envelope protein of ASFV, can significantly downregulated NF-κB activation induced by IL-1β or TNFα. The overexpression of pH108R suppresses transcription of several proinflammatory cytokines such as IL-6， IL-8，and TNFα induced by IL-1β or TNFα in HEK293T cells. Consistently, the levels of phosphorylated p65 and IκBα were decreased in pH108R overexpression cells after IL-1β and TNFα stimulation. In addition，Transcriptome sequencing showed that it could significantly down-regulate the expression of TNF-induced immune and inflammatory genes in PK-15 cells. Collectively, our study indicates that ASFV pH108R markedly suppresses NF-κB activation stimulated by IL-1β and TNFα, clarifies the immunosuppressive activity of pH108R and provides a new perspective for analyzing the immune escape of African swine fever.
2025-09-26 | GSE287718 | GEO