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RSAD2/VIPERIN and CMPK2 Coordinate an Immunometabolic Response to Epstein-Barr Virus

GSE319301 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/06/01 Platform GPL30173
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: 6 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)
Epstein-Barr Virus (EBV) infection and reactivation in B-lymphocytes is tightly regulated by host antiviral response genes. In the present study, we identify interferon stimulated genes RSAD2 (radical S-adenosyl methionine domain-containing 2) and CMPK2 (Cytidine/Uridine Monophosphate Kinase 2) as key modulators of EBV expression and cellular response during EBV infection and reactivation.
Read the full summary ↓
EBV primary infection and reactivation lead to a coordinated upregulation of RSAD2 and CMPK2. Depletion of RSAD2 reduced cell viability and limited EBV reactivation, while depletion of CMPK2 led to reactivation of EBV lytic gene expression during latency. Transcriptomic analysis revealed that RSAD2 and CMPK2 have overlapping functions in regulating IFN-signaling pathways, as well as oxidative phosphorylation, protein translation, and unfolded protein response during reactivation. Despite distinct subcellular localizations, RSAD2 at the Endoplasmic Reticulum (ER), and CMPK2 in mitochondria, both genes converge on shared immunometabolic pathways, including control of Gasdermin D (GSDMD) associated pyroptosis and ATF-4 associated unfolded protein response (UPR). EBV reactivation induced formation of antiviral ribonucleotide ddhCTP during lytic EBV reactivation which was strictly dependent on RSAD2. Knockdown of RSAD2 and CMPK2 had significant effects on global metabolites consistent with a remodeling of glycolysis, fatty acid biosynthesis and degradation of superoxides. These observations demonstrate that RSAD2-CMPK2 function in a coordinated ER-mitochondria stress-Interferon signaling axis that shapes EBV reactivation and host immune control, including a novel layer of immunometabolic regulation modulating viral latency and reactivation.
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 GSE319301_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: 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 PRJNA1422798 and SRA study SRP676588. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
shControl, Uninduced, ×3 shRSAD2, Uninduced, ×3 shCMPK2, Uninduced, ×3 shControl, Induced, ×3 shRSAD2, Induced, ×3 shCMPK2, Induced, ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 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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