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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 [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.

2024-07-31 | GSE272666 | GEO

Genetic Architecture of Smoking and Smoking Cessation

Project description:Genetic Architecture of Smoking and Smoking Cessation

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Cannabis smoking is associated with advanced epigenetic age

Project description:Cannabis use has been controversial, largely having been designated a controlled substance over the last century. The link between cannabis smoking and disease pathogenesis may best be explored through DNA methylation, an epigentic mechanism. We investigated the relationship between epigenetic age and cannabis smoking in participants within the Canadian Cohort of Obstructive Lung Disease (CanCOLD) cohort (n=93) (ClinicalTrials.gov identifier NCT00920348). Blood samples were profiled for DNA methylation using the Illumina MethylationEPIC BeadChipv1 at two separate laboratories and the blood epigenetic age of each sample was calculated using the Clock Foundation tool (https://dnamage.clockfoundation.org). An ANOVA was used to identify differences in the age acceleration residuals associated with cannabis smoking status (never, former, and current), adjusted for chronological age, sex, body mass index (BMI), batch, cigarette smoking status, and the first two principal components of blood cell proportions. Our observations indicated that current cannabis smoking and higher joint-years exposure are associated with epigenetic age acceleration; cessation, however, may help to normalize in part this age acceleration.

2024-07-01 | GSE255929 | GEO

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