Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407445 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6040940_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040940_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040941_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040941_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040942_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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Project description:ILC1 confer early host protection at initial sites of viral infection
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Project description:ILC1 confer early host protection at initial sites of viral infection [RNA-Seq]
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Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.
2019-05-02 | GSE128906 | GEO
Project description:We show that tissue-resident ILC1 serve a non-redundant early role in host immunity through rapid production of interferon (IFN)-γ following mouse cytomegalovirus (MCMV) infection.
2017-11-01 | GSE103901 | GEO
Project description:We show that tissue-resident ILC1 serve a non-redundant early role in host immunity through rapid production of interferon (IFN)-γ following mouse cytomegalovirus (MCMV) infection.
2017-11-01 | GSE103900 | GEO
Project description:Background and Aims: Complex host-virus interactions account for HBV-specific T and B cells dysfunction and the persistence of the viral cccDNA mini-chromosome, key features of HBV chronicity and challenges for HBV cure. The extent of HBV impact on liver transcriptome remains controversial. Transcriptional activation in eukaryotic cells has been tightly linked with disruption of nucleosome organization at accessible genomic sites of remodeled chromatin. We used ATAC-seq (Assay for Transposase Accessible Chromatin followed by high throughput sequencing) to detect early changes in chromatin accessibility in HBV-infected Primary Human Hepatocytes (PHHs). Results. ATAC-seq analysis revealed that after HBV infection an increasing number of genomic sites change their chromatin accessibility over time with a prevalent global reduction of accessibility (that is) partially prevented by inhibiting HBV transcription and replication. Motif Enrichment Analysis identified several TF involved in liver cell identity, glucose and lipid metabolism as potential regulators of differentially accessible genes 72h post-infection, when cccDNA transcription and viral replication are established. ATAC-seq and RNA-seq integration confirmed HBV infection impact on liver metabolism, the early establishment of a premalignant phenotype and identified a 39-genes liver iron signature modulated by chromatin accessibility changes. The upregulation of iron uptake genes translates in a significant increase of iron content in HBV-infected PHHs whereas iron chelation results in a drastic inhibition of cccDNA transcription and viral replication. Conclusions. Altogether our results show that HBV infection impacts on host cell chromatin landscape and specific transcriptional programs and that HBV modulates intracellular available iron to boost its replication.
2025-05-29 | GSE240183 | GEO
Project description:Background and Aims: Complex host-virus interactions account for HBV-specific T and B cells dysfunction and the persistence of the viral cccDNA mini-chromosome, key features of HBV chronicity and challenges for HBV cure. The extent of HBV impact on liver transcriptome remains controversial. Transcriptional activation in eukaryotic cells has been tightly linked with disruption of nucleosome organization at accessible genomic sites of remodeled chromatin. We used ATAC-seq (Assay for Transposase Accessible Chromatin followed by high throughput sequencing) to detect early changes in chromatin accessibility in HBV-infected Primary Human Hepatocytes (PHHs). Results. ATAC-seq analysis revealed that after HBV infection an increasing number of genomic sites change their chromatin accessibility over time with a prevalent global reduction of accessibility (that is) partially prevented by inhibiting HBV transcription and replication. Motif Enrichment Analysis identified several TF involved in liver cell identity, glucose and lipid metabolism as potential regulators of differentially accessible genes 72h post-infection, when cccDNA transcription and viral replication are established. ATAC-seq and RNA-seq integration confirmed HBV infection impact on liver metabolism, the early establishment of a premalignant phenotype and identified a 39-genes liver iron signature modulated by chromatin accessibility changes. The upregulation of iron uptake genes translates in a significant increase of iron content in HBV-infected PHHs whereas iron chelation results in a drastic inhibition of cccDNA transcription and viral replication. Conclusions. Altogether our results show that HBV infection impacts on host cell chromatin landscape and specific transcriptional programs and that HBV modulates intracellular available iron to boost its replication.
2025-05-29 | GSE239860 | GEO
Project description:Influenza and other respiratory viral pathogens are leading causes of mortality and morbidity. We previously demonstrated that circadian rhythms confer temporal protection from influenza infection. Here, we investigated whether this protection requires rhythmic function after the initial infection by manipulating environmental cycles. We demonstrate that disrupting environmental lighting cues within a critical window of vulnerability abrogates time-of-day specific protection. This poor outcome is mediated by a dysregulated immune response, evidenced by the accumulation of inflammatory monocytes and CD8+ cells in the lungs and a transcriptomic profile indicative of an exaggerated immune response. Disruption of the light cycle does not affect outcomes in a clock mutant, indicating that it acts by compromising endogenous timekeeping. Importantly, rhythmic meal timing mitigates the adverse effects of disrupted light cycles, suggesting that external cycling cues, which act through different body clocks, can substitute for each other. Our findings highlight the crucial interplay between environmental factors and endogenous clocks in shaping influenza outcomes, offering significant translational potential for improving the care of critically ill patients with respiratory viral infections.
2025-07-23 | GSE296722 | GEO
Project description:This ordinary differential equation model is described in the following article:
"Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host"
G. Michael Lavigne, Hayley Russell, Barbara Sherry and Ruian Ke
DOI: 10.1098/rspb.2020.3002
Comment:
This model is based on the ordinary differential equations of the non-spatial model of well-mixed viral infection stated in the manuscript (Eq. 2.1 in the article).
Abstract:
The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.
2024-09-02 | BIOMD0000001021 | BioModels
Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. We showed that MV130 induces long term heterologous protection against viral respiratory infections in mice. Moreover, intranasal administration of MV130 provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. As trained immunity acts via modulation of hematopoietic stem and progenitor cells (Kaufmann et al., 2018; Mitroulis et al., 2018) we hypothesized that MV130 could confer systemic long-term protection through reprogramming of hematopoietic precursors. For that we measured the chromatin accessibility landscape in multipotent progenitors (MPPs) coming from mice treated with MV130 or its excipient using ATAC-seq.
2021-11-10 | GSE183486 | GEO