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Smoking-associated DNA methylation features link to HIV outcomes

ABSTRACT: Smoking-associated DNA methylation features link to HIV outcomes

PROVIDER: PRJNA483450 | ENA |

REPOSITORIES: ENA

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Smoking-associated DNA methylation features link to HIV outcomes [Infinium MethylationEPIC]

Project description:Smoking is common in people who live with HIV infection and has significant adverse effects on HIV outcomes. The impacts of smoking on methylome has been well established in non-HIV populations. However, the smoking’s effects on host methylome in HIV-positive population has not been investigated and it is unknown if smoking-associated DNA methylation link to HIV outcomes. In this study, we applied machine learning methods selected smoking-associated DNA methylation features to predict HIV related frailty and mortality.

2019-07-23 | GSE117860 | GEO

Smoking-associated DNA methylation features link to HIV outcomes [HumanMethylation450 BeadChip]

2019-07-23 | GSE117859 | GEO

Smoking-associated DNA methylation features link to HIV outcomes [Infinium MethylationEPIC]

Project description:Smoking-associated DNA methylation features link to HIV outcomes [Infinium MethylationEPIC]

| PRJNA483457 | ENA

Smoking-associated DNA methylation features link to HIV outcomes [HumanMethylation450 BeadChip]

Project description:Smoking-associated DNA methylation features link to HIV outcomes [HumanMethylation450 BeadChip]

| PRJNA483456 | ENA

Smoking-associated DNA methylation features link to HIV outcomes

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-23 | GSE117861 | GEO

Association of smoking with neurocognition, inflammatory and myeloid cell activation profiles in people with HIV on ART

Project description:Objective: People with HIV (PWH) experience excess comorbidities, including neurocognitive disorders, which are linked to inflammation, particularly monocyte-macrophage activation. Smoking contributes to morbidity and mortality in well-treated PWH. We investigated associations between smoking, neurocognitive function, and inflammation in PWH on ART. Design: We used baseline data on cognition and inflammation from a randomized treatment study among smoking and non-smoking PWH. Participants completed 4 neurocognitive tests (7 measures), with a composite score as the primary measure. Inflammatory markers were plasma sCD14, sCD163, and CCL2/MCP-1; %CD14+ monocytes expressing CD16, CD163, and CCR2; and %CD8+ T cells co-expressing CD38/HLA-DR. Exploratory analyses included a plasma cytokine/chemokine panel, hsCRP, neurofilament light chain (NFL) and monocyte transcriptomes by RNAseq. Results: We recruited 58 PWH (26 smokers, 32 non-smokers). Mean composite and individual neurocognitive scores did not differ significantly by smoking status except for the color shape task; smokers exhibited worse cognitive flexibility, with adjusted mean times 317.2 (95%CI 1.4, 632.9) msec longer than non-smokers. Smokers had higher plasma sCD14 than non-smokers (median(IQR) 1820(1678, 2105) versus 1551(1284, 1760) ng/ml, p=0.009). Other inflammatory markers were not significantly different between smokers and non-smokers. Monocyte transcriptomes showed several functions, regulators and gene sets that differed by smoking status. Conclusions: sCD14, a marker of monocyte activation, is elevated in PWH who smoke. While neurocognitive measures and other inflammatory markers did not generally differ, these data implicate smoking-related myeloid activation and monocyte gene dysregulation in the HIV/smoking synergy driving HIV-associated comorbidities.

2025-01-02 | GSE274848 | GEO

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Project description:Drosophila melanogaster link, link, is differentially expressed in 6 experiment(s);

| FBgn0033855 | ExpressionAtlas

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Project description:Drosophila melanogaster link, link, is expressed in 4 baseline experiment(s);

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Distinguishing smoking related lung disease phenotypes via imaging and molecular features

Project description:Distinguishing smoking related lung disease phenotypes via imaging and molecular features

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Transcriptional and methylation outcomes of didehydro-Cortistatin A use in HIV-1 infected CD4+T cells

Project description:Ongoing viral transcription from the reservoir of long-lived CD4+ T cells containing integrated HIV-1 DNA presents a barrier to cure and associates with poorer health outcomes for people living with HIV, including chronic immune activation and inflammation. We previously reported that didehydro-Cortistatin A (dCA), an HIV-1 Tat inhibitor, blocks HIV-1 transcription. We sought to extend this work and examine the impact of dCA on host immune CD4+ T cell transcriptional and epigenetic states. Here, we performed a comprehensive analysis of genome-wide transcriptomic and DNA methylation profiles upon long-term dCA-treatment of primary human memory CD4+ T cells. dCA prompted specific transcriptional and DNA methylation changes in cell cycle, histone, interferon-response and T cell lineage transcription factor genes, through inhibition of both HIV-1 and Mediator kinases. These alterations establish a tolerogenic Treg/Th2 phenotype, reducing viral gene expression and mitigating inflammation in primary CD4+T cells during HIV-1 infection. Additionally, dCA suppresses expression of lineage-defining transcription factors for Th17 and Th1 cells, critical HIV-1 targets and reservoirs. dCA’s benefits thus extend beyond viral transcription inhibition, modulating immune cell landscape to limit HIV-1 acquisition and inflammatory environment linked to HIV-infection.

2024-07-31 | GSE272666 | GEO

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