Ontology highlight
ABSTRACT:
PROVIDER: PRJNA859002 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20218712_1.fastq.gz | Fastqsanger.gz | |||
| SRR20218713_1.fastq.gz | Fastqsanger.gz | |||
| SRR20218714_1.fastq.gz | Fastqsanger.gz | |||
| SRR20218715_1.fastq.gz | Fastqsanger.gz | |||
| SRR20218716_1.fastq.gz | Fastqsanger.gz |
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Project description:Salmonella Heidelberg is currently the 9th common serovar and has more than twice the average incidence of blood infections in Salmonella. A recent Salmonella Heidelberg outbreak in chicken infected 634 people during 2013-2014, with a hospitalization rate of 38% and an invasive illness rate of 15%. While the company’s history suggested longstanding sanitation issues, the strains’ characteristics which may have contributed to the outbreak are unknown. We hypothesized that the outbreak strains of S. Heidelberg might possess enhanced stress tolerance or virulence capabilities. Consequently, we obtained nine food isolates collected during the outbreak investigation and several reference isolates and tested their tolerance to processing stresses, their ability to form biofilms, and their invasiveness in vitro. We further performed RNA-sequencing on three isolates with varying heat tolerance to determine the mechanism behind our isolates’ enhanced heat tolerance. Ultimately, we determined that (i) many Salmonella Heidelberg isolates associated with a foodborne outbreak have enhanced heat resistance (ii) Salmonella Heidelberg outbreak isolates have enhanced biofilm-forming ability under stressful conditions, compared to the reference strain (iii) exposure to heat stress may also increase Salmonella Heidelberg isolates’ antibiotic resistance and virulence capabilities and (iv) Salmonella Heidelberg outbreak-associated isolates are primed to better survive stress and cause illness. This data helps explain the severity and scope of the outbreak these isolates are associated with and can be used to inform regulatory decisions on Salmonella in poultry and to develop assays to screen isolates for stress tolerance and likelihood of causing severe illness.
2018-09-01 | GSE103418 | GEO
Project description:ASFV poses a continuing threat to the pig industry in Europe as broadly applicable vaccines are not available. Variations within the ASFV genome resulted in the emergence of attenuated strains with low or moderate virulence, however, the molecular basis of the differences in virulence is not known. To reveal virulence-associated protein expression patterns, we have analyzed the proteomes of the natural target cells of ASFV, primary porcine macrophages, after infection with two genotype II ASFV strains displaying high (“Armenia 2008”) and moderate (”Estonia 2014”) virulence using quantitative mass spectrometry. Very similar expression patterns were observed for the viral genes. In addition to the canonical ASFV proteins, twelve novel protein products from recently described transcripts could be confirmed in both isolates. Pathway analysis showed that both isolates evoked a similar host proteome response despite their difference in virulence. However, subtle differences in the manipulation of the proteins involved in the proinflammatory response mediated by the MAPK14/p38 signalling cascade were observed.
2023-01-05 | PXD036402 | Pride
Project description:Clonal emergence is a major driver for changes in bacterial disease epidemiology. Recently, it has been proposed that episodic emergence of novel, hypervirulent clones of group A Streptococcus (GAS) results from horizontal gene transfer (HGT) and recombination events leading to increased expression of the cytotoxins Nga (NADase) and SLO (streptolysin O). We previously described a gene fusion event involving the gene encoding the GAS M protein (emm) and an adjacent M-like protein (enn) in the emm4 GAS population, a GAS emm type that lacks the hyaluronic acid capsule. Using whole genome sequencing of a temporally and geographically diverse set of 1,127 isolates, we discovered that the North American emm4 GAS population has undergone clonal replacement with emergent GAS strains completely replacing historical isolates by 2017. Emergent emm4 GAS strains were defined by a handful of small genetic variations, including the emm-enn gene fusion, and showed a marked in vitro growth defect compared to historical strains. In contrast to other previously described GAS clonal emergence events, emergent emm4 GAS lacked significant HGT events and showed no significant increase in transcript levels of nga/slo toxin gene via RNA sequencing and quantitative real-time PCR analysis relative to historic strains. Despite the in vitro growth differences, emergent emm4 GAS strains demonstrated hypervirulence in mouse and ex vivo growth in human blood compared to historical strains. Thus, these data detail the emergence and dissemination of a hypervirulent acapsular GAS clone defined by small genetic variation thereby defining a novel model for GAS strain replacement.
2021-05-05 | GSE160737 | GEO
Project description:Long noncoding RNAs (lncRNAs) participate in regulating many biological processes. However, their roles in African swine fever virus(ASFV) pathogenicity are largely unknown. Here, we analyzed the expression profile of lncRNAs and mRNAs in the ASFV-infected or uninfected PAMs by high-throughput sequencing
2024-07-27 | GSE180939 | GEO
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:An array analysis of C. gattii (C. bacillosporus), intended to identify loci associated with the hypervirulence of the Vancouver Island Outbreak (VIO). 23 C. gattii isolates, representing both VIO strains and control strains, were grown for 24 hours in mammalian macrophages. RNA was isolated and gene expression for each strain quantified relative to pooled RNA from all 23 samples. Linear regression was used to identify loci showing positive or negative correlation with "intracellular proliferation rate", a proxy measure for virulence. Data from this analysis is included in Ma et al, 2009, PNAS 106(31) 12980-12985. The abstract is included below. In 1999, the population of Vancouver Island, Canada, began to experience an outbreak of a fatal fungal disease caused by a highly virulent lineage of Cryptococcus gattii. This organism has recently spread to the Canadian mainland and Pacific Northwest, but the molecular cause of the outbreak remains unknown. Here we show that the Vancouver Island outbreak (VIO) isolates have dramatically increased their ability to replicate within macrophages of the mammalian immune system in comparison with other C. gattii strains. We further demonstrate that such enhanced intracellular parasitism is directly linked to virulence in a murine model of cryptococcosis, suggesting that this phenotype may be the cause of the outbreak. Finally, microarray studies on 24 C. gattii strains reveals that the hypervirulence of the VIO isolates is characterized by the up-regulation of a large group of genes, many of which are encoded by mitochondrial genome or associated with mitochondrial activities. This expression profile correlates with an unusual mitochondrial morphology exhibited by the VIO strains after phagocytosis. Our data thus demonstrate that the intracellular parasitism of macrophages is a key driver of a human disease outbreak, a finding that has significant implications for a wide range of other human pathogens.
2009-08-07 | GSE17052 | GEO
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.
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Project description:<p>African swine fever virus (ASFV) is an infectious disease with a mortality rate of nearly 100% in pigs; however, no safe commercial vaccines or antiviral drugs are currently available, which seriously threatens the global pig industry. Therefore, effective biologicals against ASFV are urgently needed. Here, we screened 138 <em>Bacillus subtilis</em> strains, four of which evidently inhibited ASFV replication in vitro. Pigs fed with biologics of different types from the four <em>B. subtilis</em> strains showed reduced pathological changes and viral loads in tissues, with a survival rate of up to 100%. The antiviral activity of <em>B. subtilis</em> was attributed to small-molecule metabolites, rather than to secretory proteins. A total of 169 small molecules were obtained from the metabolites of <em>B. subtilis</em> using LC-MS/MS, arctiin and genistein, which showed the highest inhibition efficiency, suppressing ASFV proliferation at the mid-stage of infection. These molecules acted as competitive inhibitors by complexing the ATP-binding domain of viral topoisomerase II, as demonstrated using molecular docking, biolayer interferometry binding and a competitive decatenation assay, thereby disrupting the catalytic activity of the enzyme and inhibiting ASFV replication. Furthermore, pigs administered arctiin and genistein orally showed decreased mortality and tissue damage. Collectively, these results suggest that the four <em>B. subtilis</em> strains screened may be preventative biologicals against ASFV infection. Our findings pave the way for ASFV prevention and control strategies in the pig industry to curb the economic losses caused by the disease.</p><p><br></p><p><strong>IMPORTANCE:</strong> African swine fever virus (ASFV) is a highly fatal swine disease that severely affects the pig industry. Although ASFV has been prevalent for more than 100 years, effective vaccines or antiviral strategies are still lacking. In this study, we identified four <em>Bacillus subtilis</em> strains that inhibited ASFV proliferation <em>in vitro</em>. Pigs fed with liquid biologicals or powders derived from four <em>B. subtilis</em> strains mixed with pellet feed showed reduced morbidity and mortality when challenged with ASFV. Further analysis showed that the antiviral activity of <em>B. subtilis</em> was based on its metabolites arctiin and genistein interfering with the function of viral topoisomerase II. Our findings offer a promising new strategy for the prevention and control of ASFV that may significantly alleviate the economic losses in the pig industry.</p>
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Project description:To systematically delineate the Protein–Protein Interaction (PPI) network between ASFV and host immune pathway proteins, and ASFV-ASFV PPI, we used the recombination-based library vs library high-throughput yeast two-hybrid (RLL-Y2H) screening system.
2023-10-23 | GSE220585 | 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