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Virally encoded interleukin-6 (vIL-6) coordinates with human IL-6 to modulate cytokine expression during KSHV infection

GSE309397 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2025/12/04 Platform GPL18573
At a glance

RNA-seq (gene expression) · human · 24 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
24 samples: 8 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.
Paper
Virally encoded interleukin-6 (vIL-6) coordinates with human IL-6 to modulate cytokine expression during KSHV infectionbioRxiv : the preprint server for biology · 2025
Summary (written by the submitters)
Kaposi Sarcoma-Associated Herpesvirus (KSHV) is characterized by its ability to establish lifelong infections that can lead to disease in immunocompromised individuals. Understanding the complex interactions between KSHV, the host cellular machinery, and the immune response is essential for unraveling the mechanisms underlying viral persistence and pathogenesis.
Read the full summary ↓
KSHV extensively remodels the host gene expression landscape by inducing widespread RNA decay via the viral endoribonuclease SOX. While the vast majority of cellular mRNAs are degraded by SOX, select transcripts including Interleukin 6 (IL-6) escape degradation. Interestingly, KSHV encodes a viral homolog of the IL-6 transcript, known as viral interleukin-6 (vIL-6). Given the importance of IL-6 for KSHV biology and its ability to escape SOX-mediated decay, we explored how vIL-6 expression is regulated upon KSHV infection. Our data demonstrate that unlike IL-6, vIL-6 3’UTR does not provide protection from SOX degradation, yet vIL-6 mRNA steady state levels remain high throughout KSHV lytic cycle, suggesting a distinct transcriptional regulation. To assess the contributions of vIL-6 and IL-6 in modulating host genes expression, inflammatory signaling and KSHV-driven pathogenesis, we used a vIL-6 null viral mutant combined with an IL-6 knock down to perform transcriptomic analyses. This analysis revealed that depletion of IL-6, vIL-6 or both results in distinct alterations of the host gene expression environment, with differential effects on chemokine signaling and related pathways as well as a synergetic effect when both IL-6 and vIL-6 are present. Furthermore, functional assays confirmed vIL-6 alone is sufficient to activate key signaling pathways and pro-inflammatory responses, including the JAK/STAT pathway. Collectively, our findings suggest a mechanistic synergy between vIL-6 and IL-6 that may enhance KSHV-mediated immune modulation and contribute to viral persistence and tumorigenesis.
Published in
Virally encoded interleukin-6 (vIL-6) coordinates with human IL-6 to modulate cytokine expression during KSHV infection
Bermudez Y, Schultz S, Miles J et al. · bioRxiv : the preprint server for biology 2025 · PMID 41256545 · doi:10.1101/2025.10.02.679950
This dataset
Open GSE309397 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 GSE309397_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 PRJNA1335958 and SRA study SRP629390. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41256545) ↗
Study design
8 conditions, mostly in triplicate
DeltaScramReact ×3 DeltaScramUn ×3 DeltaSiReact ×3 DeltaSiUn ×3 RevScramReact ×3 RevScramUn ×3 RevSiReact ×3 RevSiUn ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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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