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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 [HumanMethylation450 BeadChip]

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 | GSE117859 | GEO

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

2019-07-23 | GSE117860 | GEO

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 [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

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

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.

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Genetic Architecture of Smoking and Smoking Cessation

Project description:Genetic Architecture of Smoking and Smoking Cessation

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Epigenetic Features of HIV-Induced T-Cell Exhaustion Persist Despite Early Antiretroviral Therapy

Project description:T cell dysfunction occurs early following HIV infection, impacting the emergence of non-AIDS morbidities and limiting curative efforts. ART initiated during primary HIV infection (PHI) can reverse this dysfunction, but the extent of recovery is unknown. We studied 66 HIV-infected individuals treated from early PHI with up to three years of ART. Compared with HIV-uninfected controls, CD4 and CD8 T cells from early HIV infection were characterised by T cell activation and increased expression of the immune checkpoint receptors (ICRs) PD1, Tim-3 and TIGIT. Three years of ART lead to partial – but not complete – normalisation of ICR expression, the dynamics of which varied for individual ICRs. For HIV-specific cells, epigenetic profiling of tetramer-sorted CD8 T cells revealed that epigenetic features of exhaustion typically seen in chronic HIV infection were already present early in PHI, and that ART initiation during PHI resulted in only a partial shift of the epigenome to one with more favourable memory characteristics. These findings suggest that although ART initiation during PHI results in significant immune reconstitution, there may be only partial resolution of HIV-related phenotypic and epigenetic changes.

2023-07-19 | GSE237729 | GEO

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