Circulating miRNA levels in HIV infection vs non-infected controls
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA900562 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22262600.fastq.gz | Fastqsanger.gz | |||
| SRR22262601.fastq.gz | Fastqsanger.gz | |||
| SRR22262602.fastq.gz | Fastqsanger.gz | |||
| SRR22262603.fastq.gz | Fastqsanger.gz | |||
| SRR22262604.fastq.gz | Fastqsanger.gz |
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Project description:HIV infection produces a chronic inflammation which leads to early aging of people living with HIV. Even though antiretroviral treatments (ART) have significantly increased HIV patient survival, an underlying chronic inflammation persists leading to HIV-related comorbidities. In this context, changes in microRNAs (miRNAs) expression may contribute to this inflammatory response. This study aims to detect differential expression of circulating miRNAs in treatment-naïve HIV individuals compared to uninfected controls and evaluation of altered miRNAs after one year of ART. Serum miRNAs from patients and controls were analysed using next generation sequencing.
2023-12-31 | GSE217795 | GEO
Project description:Mechanisms that may allow circulating monocytes to persist as CD4 T cells diminish in HIV-1 infection have not been investigated. We have characterized steady-state gene expression signatures in circulating monocytes from HIV-infected subjects and have identified a stable anti-apoptosis gene signature comprised of 38 genes associated with p53, CD40L, TNF and MAPKinase signaling networks. The significance of this gene signature is indicated by our demonstration of cadmium chloride- or Fas ligand-induced apoptosis resistance in circulating monocytes in contrast to increasing apoptosis in CD4 T cells from the same infected subjects. As potential mechanisms in vivo, we show that monocyte CCR5 binding by HIV-1 virus or agonist chemokines serve as independent viral and host modulators resulting in increased monocyte apoptosis resistance in vitro. We also show evidence for concordance between circulating monocyte apoptosis-related gene expression in HIV-1 infection in vivo and available datasets following viral infection or envelope exposure in monocyte derived macrophages in vitro. The identification of in vivo gene expression associated with monocyte resistance to apoptosis is of relevance to AIDS pathogenesis since it would contribute to: (1) maintaining viability of infection targets and long-term reservoirs of HIV-1 infection in the monocyte/macrophage populations, and (2) protecting a cell subset critical to host survival in spite of sustained high viral replication. Keywords: two group study design 33 samples hybridized, including 13 HIV-1 Patients, 12 Healthy Controls and 4 HIV-1 Patients and 4 Controls followed 6 months later
2010-06-25 | E-GEOD-14542 | biostudies-arrayexpress
Project description:Mechanisms that may allow circulating monocytes to persist as CD4 T cells diminish in HIV-1 infection have not been investigated. We have characterized steady-state gene expression signatures in circulating monocytes from HIV-infected subjects and have identified a stable anti-apoptosis gene signature comprised of 38 genes associated with p53, CD40L, TNF and MAPKinase signaling networks. The significance of this gene signature is indicated by our demonstration of cadmium chloride- or Fas ligand-induced apoptosis resistance in circulating monocytes in contrast to increasing apoptosis in CD4 T cells from the same infected subjects. As potential mechanisms in vivo, we show that monocyte CCR5 binding by HIV-1 virus or agonist chemokines serve as independent viral and host modulators resulting in increased monocyte apoptosis resistance in vitro. We also show evidence for concordance between circulating monocyte apoptosis-related gene expression in HIV-1 infection in vivo and available datasets following viral infection or envelope exposure in monocyte derived macrophages in vitro. The identification of in vivo gene expression associated with monocyte resistance to apoptosis is of relevance to AIDS pathogenesis since it would contribute to: (1) maintaining viability of infection targets and long-term reservoirs of HIV-1 infection in the monocyte/macrophage populations, and (2) protecting a cell subset critical to host survival in spite of sustained high viral replication. Keywords: two group study design
2009-03-01 | GSE14542 | GEO
Project description:Background: HIV infection is associated with impaired gas transfer in the lung as indicated by a low diffusing capacity (DLCO). Mechanisms for reduced DLCO in the setting of HIV infection are not well understood. We hypothesized that HIV-associated gas exchange impairment is indicative of system-wide perturbations that could be reflected by alterations in peripheral blood gene expression. Methods: A total of 40 HIV-infected (HIV+) and uninfected (HIV-) men with preserved versus reduced DLCO were selected from a larger cohort study of lung function. All subjects were current smokers and those with acute illness, lung diseases other than COPD or asthma were excluded. Total RNA was extracted from peripheral blood leukocytes (PBLs) and hybridized to whole-genome microarrays. Gene set enrichment analysis (GSEA) was performed between HIV+ vs. HIV- subjects with preserved DLCO and those with impaired DLCO to identify differentially activated pathways. Results: Using pathway-based analyses we found that in subjects with preserved DLCO, HIV infection is associated with activation of processes involved in immunity, cell cycle, and apoptosis. When we applied a similar analysis to subjects with low DLCO, we identified a much broader repertoire of inflammatory and immune-related pathways in HIV+ patients relative to HIV- subjects, with up-regulation of multiple interleukin pathways, interferon signaling, Toll-like receptor signaling, and T cell/B cell receptor signaling. We confirmed elevated circulating levels of IL-6 in HIV+ patients with reduced DLCO relative to the other groups. Conclusions: Our findings reveal that PBLs of subjects with HIV infection and low DLCO are distinguished by widespread enrichment of immuno-inflammatory programs. Activation of these pathways may alter the biology of circulating leukocytes and play a role in the pathogenesis of HIV-associated pulmonary gas exchange impairment. Total RNA was isolated from peripheral blood leukocytes in four subject groups: 1. HIV-, low DLCO (N = 11); 2. HIV+, low DLCO (N = 10); 3. HIV-, preserved DLCO (N = 9); 4. HIV+, preserved DLCO (N = 9). Each sample was hybridized to an Affymetrix PrimeView Human Gene Expression microarray for a total of 39 experiments.
2016-04-01 | E-GEOD-76403 | biostudies-arrayexpress
Project description:This study used TaqMan low-density arrays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status. Blood samples were from six uninfected controls, six HIV-1 elite suppressors with undetectable viral load, and six viremic HIV-1-infected patients.
2012-02-22 | E-GEOD-33492 | biostudies-arrayexpress
Project description:This study used TaqMan low-density arrays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status.
2012-02-22 | GSE33492 | GEO
Project description:This study used the NanoString nCounter hybridization system and nCounter miRNA expression assays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status. Blood samples were from eight uninfected controls, seven HIV-1 elite suppressors with undetectable viral load, and six viremic HIV-1-infected patients.
2012-02-22 | E-GEOD-33387 | biostudies-arrayexpress
Project description:Background: HIV infection is associated with impaired gas transfer in the lung as indicated by a low diffusing capacity (DLCO). Mechanisms for reduced DLCO in the setting of HIV infection are not well understood. We hypothesized that HIV-associated gas exchange impairment is indicative of system-wide perturbations that could be reflected by alterations in peripheral blood gene expression. Methods: A total of 40 HIV-infected (HIV+) and uninfected (HIV-) men with preserved versus reduced DLCO were selected from a larger cohort study of lung function. All subjects were current smokers and those with acute illness, lung diseases other than COPD or asthma were excluded. Total RNA was extracted from peripheral blood leukocytes (PBLs) and hybridized to whole-genome microarrays. Gene set enrichment analysis (GSEA) was performed between HIV+ vs. HIV- subjects with preserved DLCO and those with impaired DLCO to identify differentially activated pathways. Results: Using pathway-based analyses we found that in subjects with preserved DLCO, HIV infection is associated with activation of processes involved in immunity, cell cycle, and apoptosis. When we applied a similar analysis to subjects with low DLCO, we identified a much broader repertoire of inflammatory and immune-related pathways in HIV+ patients relative to HIV- subjects, with up-regulation of multiple interleukin pathways, interferon signaling, Toll-like receptor signaling, and T cell/B cell receptor signaling. We confirmed elevated circulating levels of IL-6 in HIV+ patients with reduced DLCO relative to the other groups. Conclusions: Our findings reveal that PBLs of subjects with HIV infection and low DLCO are distinguished by widespread enrichment of immuno-inflammatory programs. Activation of these pathways may alter the biology of circulating leukocytes and play a role in the pathogenesis of HIV-associated pulmonary gas exchange impairment.
2016-04-01 | GSE76403 | GEO
Project description:This study used the NanoString nCounter hybridization system and nCounter miRNA expression assays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status.
2012-02-22 | GSE33387 | GEO
Project description:The lack of available biomarkers to diagnose and predict different stages of liver disease with a non-invasive strategy is currently one of the main challenges that clinicians are facing. Recent evidence indicates that the plasma levels of specific microRNAs (miRNAs) may be significantly altered in patients with liver injury, including human immunodeficiency virus type 1 (HIV-1) infected patients. Large-scale deep sequencing analysis of small RNA expression was performed on plasma samples from 46 HIV-1/hepatitis C virus (HCV) co-infected patients that did not exhibit liver fibrosis at the time of sampling. A total of 1065 different miRNAs were identified. After a mean of 10.3 years, 26 of the former patients developed liver fibrosis (stage F2-4) and 20 remained without signs of liver fibrosis (stage F0-1). We identified a signature of seven miRNAs, 100-5p, 192-5p, 99a-5p, 122-5p, 125b-2-3p, 1246 and 194-5p, that highly correlated with patients progressing to liver fibrosis. These seven miRNAs detected liver fibrosis progression with an area under curve (AUC) of 0.910-0.806. The two miRNAs, 100-5p and 192-5p, displaying the best AUC values, yielded both a sensitivity of 88% and a specificity of 85% for liver fibrosis progression. Our results demonstrate the predictive potential of circulating levels of miRNAs to foresee liver fibrosis progression even before liver fibrosis or significant clinical differences such as liver transaminases or platelets are detectable. Thus, our study might help in predicting the progression of liver injury in HIV-1-infected patients.
2021-11-08 | GSE161845 | GEO