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The HIV-1 Vpr R77Q mutant alters host apoptotic gene regulation in CD4+ T cells

GSE319139 Homo sapiens (human) RNA-seq (gene expression) 33 samples Submitted 2026/05/20 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 33 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
33 samples: 11 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
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.
Summary (written by the submitters)
HIV-1 viral protein R (Vpr) is a multifunctional protein central to HIV-1 pathogenesis and progression to AIDS. Polymorphisms in vpr have been linked to varying rates of HIV-1 progression. Of note is the HIV-1 Vpr R77Q mutant, associated with delayed progression to AIDS. We previously demonstrated that the R77Q mutant promotes a non-inflammatory, apoptotic phenotype in CD4+ T cells.
Read the full summary ↓
To investigate the mechanism underlying the R77Q-induced apoptotic phenotype, we performed RNA sequencing on a CD4+ T cell line, HUT78, infected with either a replication-competent wild-type strain (NL4-3) or the R77Q mutant. Our results show that at 72 hours post-infection, transcriptomes were heterogeneous, and differential expression analysis identified 289 differentially expressed genes (DEGs) in the R77Q vs. WT comparison. Functional enrichment analysis revealed enriched pathways associated with apoptosis. Gene ontology (GO) terms and GO connections also revealed an apoptotic signature. Although both viral strains upregulated pro-apoptotic genes, the R77Q mutant failed to upregulate some key anti-apoptotic genes such as bcl-2, while WT-infected cells displayed upregulation of those anti-apoptotic genes. Predicted protein-protein interaction within the Bcl-2 family local network also suggests that interactions within this network were significantly different. Taken together, these findings provide a transcriptomic basis for our previous observations of enhanced apoptosis in R77Q-infected cells and highlight distinct host cell responses that may underlie delayed HIV-1 progression. These results may be useful in identifying new targets to delay AIDS progression.
This dataset
Open GSE319139 in finder → Find more human RNA-seq datasets →
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.

Series matrix ↓
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 GSE319139_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1422171 and SRA study SRP676246. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
11 conditions, mostly in triplicate
HUT78, mock control, ×3 HUT78, infected with Wild Type HIV-1 NL4-3, 4… ×3 HUT78, infected with Wild Type HIV-1 NL4-3, 8… ×3 HUT78, infected with Wild Type HIV-1 NL4-3, 1… ×3 HUT78, infected with Wild Type HIV-1 NL4-3, 2… ×3 HUT78, infected with Wild Type HIV-1 NL4-3, 7… ×3 HUT78, infected with HIV-1 vpr R77Q, 4hr, ×3 HUT78, infected with HIV-1 vpr R77Q, 8hr, ×3 +3 more

Supports a case/control comparison: 15 samples read as cases, 3 as controls.

How we read this: 11 replicated groups read from 33 sample titles; they account for 33 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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