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

GSE272666 Homo sapiens (human) DNA methylation 22 samples Submitted 2024/07/31 Platform GPL18573Platform GPL30173
At a glance

DNA methylation · human · 22 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Samples
22 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Transcriptional and methylation outcomes of didehydro-cortistatin A use in HIV-1-infected CD4(+) T cellsLife science alliance · 2024
Summary (written by the submitters)
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.
Read the full summary ↓
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.
Published in
Transcriptional and methylation outcomes of didehydro-cortistatin A use in HIV-1-infected CD4(+) T cells
Mori LP, Corley MJ, McAuley AT et al. · Life science alliance 2024 · PMID 39089880 · doi:10.26508/lsa.202402653
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE272666_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: Look for beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1137927 and SRA study SRP521054. Searching any of these in the dataset finder brings you back here.

Samples in this study

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