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ISG15-Mediated Suppression of Type I Interferon Signaling Leads to Susceptibility to Epstein-Barr Virus Infection (LCL_IFN_treatment_BulkRNAseq)

GSE298341 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/05/29 Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 18 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
18 samples: 18 samples, each with a distinct title — no replicated groupsGroups 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)
Epstein-Barr Virus (EBV), the first identified human oncogenic virus, is linked to numerous malignancies, including gastric cancer, nasopharyngeal cancer and multiple B-cell Lymphomas. However, the host-virus interactions that regulate EBV-driven cell transformation and pathogenesis remain incompletely understood. Here, employing a Cas9–ribonucleoprotein (RNP)-based screen in primary B cells, we identified 11 host factors that promote and 35 that restrict EBV-driven outgrowth.
Read the full summary ↓
Notably, ISG15, a ubiquitin-like, type I interferon-induced antiviral protein, exhibited a dependency role for growth in early stages of infection but not in LCLs. Mechanistically, we found that the regulation of free ISG15 levels greatly impacts the proliferation capacity of EBV-infected B-cells, by modulating the activation of type I IFN signaling. Finally, we identified rare germ-line variants in UBA7, the ISG15 E1 enzyme, in patients with EBV severe disorders, that impair the ISG15 conjugation process. This highlights a critical role of ISG15 in the control of EBV infections.
This dataset
Open GSE298341 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 GSE298341_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 PRJNA1268989 and SRA study SRP588260. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
18 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 18 sample titles: 18 distinct titles with little repetition. 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
Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.