B745b890-ade6-49cf-9eb3-def17308d201 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001007820 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:IL28B genotype was shown to be associated with treatment outcome of antiviral thearpy for HCV infection. We tried to clarify the molecular feature that was asocciated with IL2B genotype by comparing Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype.
2013-05-02 | GSE41804 | GEO
Project description:Hepatitis C virus (HCV) infection has been successfully managed by anti-viral therapies, however, high prevalence to severe chronic liver disease state including non-alcoholic fatty liver disease (NAFLD) is a problem encountered even after the cure of hepatitis C. Moreover, there is currently no reliable in vitro model capable of investigating host-viral interactions and monitoring the progression of viral hepatitis to chronic liver diseases. Recent organoid technology has been reported for successful infection of HCV, but there is still lack of non-parenchymal cells, which play a crucial role in disease progression. Here, we provided a novel multicellular liver organoid model using co-culture system of macrophages and liver organoids differentiated from the same cell source, human embryonic stem cells. Surprisingly, HCV infection led potent lipid accumulation in liver organoids through regulation of host lipid metabolism, which was further promoted by macrophage co-culture. Lipid enriched condition provided by longterm-treatment with fatty acid accelerated potent HCV amplification and further promotion of inflammation and fibrosis progression. Therefore, our model may be a valuable novel platform recapitulating diverse phenotypes with host-virus intercommunication and inter-cellular interactions and further progressive features of hepatitis C-associated chronic NAFLD progression of patients with HCV.
2024-05-05 | GSE229608 | GEO
Project description:Hepatitis C virus (HCV) infection has been successfully managed by anti-viral therapies, however, high prevalence to severe chronic liver disease state including non-alcoholic fatty liver disease (NAFLD) is a problem encountered even after the cure of hepatitis C. Moreover, there is currently no reliable in vitro model capable of investigating host-viral interactions and monitoring the progression of viral hepatitis to chronic liver diseases. Recent organoid technology has been reported for successful infection of HCV, but there is still lack of non-parenchymal cells, which play a crucial role in disease progression. Here, we provided a novel multicellular liver organoid model using co-culture system of macrophages and liver organoids differentiated from the same cell source, human embryonic stem cells. Surprisingly, HCV infection led potent lipid accumulation in liver organoids through regulation of host lipid metabolism, which was further promoted by macrophage co-culture. Lipid enriched condition provided by longterm-treatment with fatty acid accelerated potent HCV amplification and further promotion of inflammation and fibrosis progression. Therefore, our model may be a valuable novel platform recapitulating diverse phenotypes with host-virus intercommunication and inter-cellular interactions and further progressive features of hepatitis C-associated chronic NAFLD progression of patients with HCV.
2024-05-05 | GSE229596 | GEO
Project description:Oropouche virus (OROV) is a neglected, re-emerging arbovirus that typically causes self-limiting febrile illness but can also result in severe complications. Currently, there are no approved vaccines or treatments for OROV infection. We integrated clinical data from OROV-infected patients with human liver-derived organoid models to investigate the virus's impact on the liver and evaluate repurposed antivirals. Patient blood tests show elevated liver enzymes, suggesting OROV-associated hepatic dysfunction. OROV isolates productively infect liver organoids and induce severe cellular damage. Transcriptomic profiling reveals strong virus-host interactions, including activation of interferon-stimulated genes and cell death pathways. Pharmacological inhibition of the interferon pathway enhances OROV replication, whereas treatment with therapeutic interferon-α suppresses the infection. Molnupiravir, a clinically approved antiviral targeting viral RNA-dependent RNA polymerase, markedly inhibits OROV replication and mitigates virus-induced cytopathology. Combining molnupiravir with interferon-α resulted in synergistic antiviral activity, indicating the complementarity of virus-targeted and host-directed strategies.
2026-01-21 | GSE316780 | GEO
Project description:Infection-dependent transcriptional changes and the impact of antiviral therapy on viral replication can be measured in longitudinal human liver biopsies using single-cell RNA sequencing data
2023-06-07 | GSE234015 | GEO
Project description:A predictive model for skin fibrosis following radiotherapy in breast cancer patients was previously developed, and the rs9399005 non-coding candidate SNP associated with reduced risk was identified within a high-risk subgroup, determined by the functional RILA assay. The SNP was located downstream of the CTGF gene, but its biological function is poorly understood. The purpose of this work was to investigate its functional impact at the transcriptional level. Patient-derived dermal fibroblasts, previously genotyped for the candidate SNP, were obtained from a local biobank. Initially, six fibroblast strains for each major homozygote (CC), heterozygote (CT), and minor homozygote (TT) genotype were cultured to passage 6 and exposed to 4 Gy of irradiation or sham irradiation, but one TT fibroblast was excluded from the study due to poor quality and slow growth. Total cellular RNA was collected before irradiation (day-0) and on day-2 post-treatment for gene expression quantification using RNA-seq. After data trimming with Trimmomatic, pseudo- alignment with Kallisto and data normalization (voom function, limma), differential gene expression (DGE) analysis was carried out using the limma package (FDR<0.05). Pathway enrichment analysis was conducted using the ReactomePA package in R. Results: Few differentially expressed genes (DEGs) were identified at baseline (day-0) between the genotypes (TT vs CC: n=5; TT vs CT: n=2; CT vs CC: n=1). Transcriptome changes on day-2 were assessed by comparing irradiated and untreated samples of each genotype to the untreated CC genotype at baseline (day-0) as a common control. Significant differences in the number of DEGs were observed between fibroblasts of different genotypes (p<0.001, Chi-squared test). The highest number of DEGs on day-2 was found in CC fibroblasts (0 Gy: n=2372, 4 Gy: n=9576), while fibroblasts with the TT genotype showed significantly fewer DEGs (0 Gy: n=523, 4 Gy: n=3538), with CT fibroblasts showing intermediate levels (0 Gy: n=788, 4 Gy: n=5471). Pathway analysis after irradiation revealed similar expected responses across all genotypes, consistent with previous reports. However, pathways related to cell cycle regulation, metabolism, and signal transduction were underrepresented in TT fibroblasts at baseline but overrepresented on day-2 post-irradiation, compared to CC fibroblasts. Distinct genes were leading these under- and over-representations. A significant influence of the candidate SNP on fibroblast responses to irradiation was demonstrated, primarily through the modulation of pathways related to growth and stress regulation. Personalized approaches to managing fibrosis risk may be guided by these findings.
2026-06-25 | GSE325569 | GEO
Project description:Hepatitis B virus (HBV) is an enveloped, coated, non-cytopathic and hepatotropic partially double-stranded DNA virus in the family Hepadnaviridae genus Orthohepadnavirus. Despite significant progress in the availability of safe vaccines and antiviral therapies against HBV, it still affects approximately 257 million people worldwide and is responsible for about 887,000 deaths per year around the world [4]. HBV infection, which are associated with acute and chronic liver failure responses to viruses attacked the liver, can result in inactive carrier state, chronic hepatitis, or fulminant hepatitis and put them at high risk to develop advanced liver fibrosis and cirrhosis, and even hepatocellular cancer. Many viral factors, which could affect the disparity of clinical outcomes or disease prognosis during chronic HBV infection, have been reported in previous studies; among them, the viral genotype, as well as HBV mutations ascribing the virus to a certain phenotype, was reported to be the most important factor influencing viral pathogenesis, including the change of host immune recognition, the enhanced virulence with increased HBV replication and the facilitation of cell attachment or penetration.
2022-02-17 | PXD025968 | Pride
Project description:The objective is to study the relevance of porcine intestinal models (incl. piglet jejunums, 2D and 3D organoids derived from piglet jejunums and swine testicular cells) to study intestinal functions and to decipher the host-virus interactions during viral porcine coronavirus infection. This dataset includes RNA-seq profiling of 54 samples covering the four experimental models mentioned above, uninfected or infected with the Purdue P115 strain of the transmissible gastroenteritis virus (TGEV). Details about the experimental models: - For the in vivo model, jejunums of five week old piglets were extracted. - For the organoid model, first jejunum crypts of newborn piglets were extracted and profiled. Then, 3D organoids derived from these crypts were profiled after 5, 14 and 25 passages. Last, 2D organoids derived from 3D organoids at passage 25 were also included. - For the cellular model, we relied on swine testicular cells (ST cells) at passage 53. Samples were either mock-infected or infected with TGEV (Purdue P115 strain) at MOI 0.06 (ST cells), 0.06 and 1 (2D organoids), and 10^4.75 TCID50 (piglets). For ST cells and organoids, the total RNA was recovered at 9hpi (hours post-infection) and 24hpi. For piglets jejunums, only the latest time point was included (24hpi). For each model and each condition (control / infected), three replicates were performed.
2025-10-10 | E-MTAB-15113 | biostudies-arrayexpress
Project description:Chronic HIV-1 infection is characterized by T-cell dysregulation that is partly restored by antiretroviral therapy. Autophagy is a critical regulator of T-cell function. Here, we demonstrate a protective role for autophagy in HIV-1 disease pathogenesis. Targeted analysis of genetic variation in core autophagy gene ATG16L1 revealed the previously unidentified rs6861 polymorphism, which correlated functionally with enhanced autophagy and clinically with improved survival of untreated HIV-1-infected individuals. T cells carrying ATG16L1 rs6861(TT) genotype displayed superior antiviral immunity, evidenced by increased proliferation, revamped immune responsiveness and suppressed exhaustion/immunosenescence features. In-depth flow-cytometric and transriptional profiling revealed T-helper-cell-signatures unique to rs6861(TT) individuals with enriched regulation of pro-inflammatory networks and skewing towards immunoregulatory phenotype. Therapeutic enhancement of autophagy recapitulated the rs6861(TT)-associated traits in non-carriers. These data underscore the in vivo relevance of autophagy for longer-lasting T-cell-mediated HIV-1 control, with implications towards development of host-directed antivirals targeting autophagy to restore immune function in chronic HIV-1 infection.
2024-03-04 | GSE253769 | GEO
Project description:Patients with mpox may present with a skin rash and mild respiratory symptoms, including sore throat and cough. The genome of the mpox virus (MPXV) has been detected in throat swab specimens from some mpox patients, indicating potential involvement of the respiratory tract. In this study, we used lung organoids to investigate the effects of MPXV infection on the respiratory system by evaluating the viral replication and the infection-mediated host response. MPXV infection resulted in the accumulation of high levels of viral genomes within the cells. H&E staining showed almost no histological differences between MPXV-infected lung organoids and uninfected lung organoids. In addition, RNA-seq analysis revealed that MPXV infection did not significantly alter the gene expression levels of various lung markers. MPXV infection did not change the production of proinflammatory cytokines, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interferon-beta (IFN-β). These findings suggest that MPXV can replicate in lung organoids without significantly affecting their cellular function.
2025-11-01 | GSE287262 | GEO