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Receptor transport protein 4 (RTP4)-mediated repression of hepatitis C virus replication in mouse cells

GSE292032 Homo sapiens (human) RNA-seq (gene expression) 96 samples Submitted 2025/06/24 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 96 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
96 samples: 16 conditions, mostly with about 6 replicates eachGroups 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
Receptor transporter protein 4 (RTP4)-mediated repression of hepatitis C virus replication in mouse cellsPLoS pathogens · 2025
Summary (written by the submitters)
Hepatitis C virus (HCV) exhibits a narrow species tropism, causing robust infections only in humans and experimentally inoculated chimpanzees. The black flying fox orthologue of receptor transport protein 4 (RTP4) was previously shown to be a potent antiviral effector against several ER-replicating RNA viruses, inhibiting viral genome replication.
Read the full summary ↓
Since the murine but not the human orthologue is a potent inhibitor of HCV we aimed to analyze the potential role for RTP4 in restricting HCV replication in mice. We demonstrate that mouse RTP4 (mmRTP4) functions as a dominant inhibitor of HCV infection. Via interspecies domain-mapping, we identify the zinc-finger domain (ZFD) of murine RTP4 as the essence of its specific HCV inhibition which is consistent with prior work showing that the 3CXXC zinc finger domain of black flying fox RTP4 is necessary and sufficient for antiviral activity. Expression of mouse RTP in HCV-infected Huh7 cells profoundly reduced HCV RNA, NS5A protein production and virion release demonstrating that mmRTP4 can also disrupt already established HCV replication complexes. Bulk RNAseq analysis of HCV-infected samples did not reveal any characteristic antiviral transcriptional signatures following mmRTP4 transduction, indicating that this antiviral activity cannot be readily attributed to induction of an antiviral response. In situ proximity ligation revealed that murine RTP4 associates with the HCV NS5A protein significantly more than human RTP4 during infection. Disrupting RTP4 expression in mice expressing humanized alleles of CD81 and occludin (OCLN) – the species specific cellular factors mediating HCV uptake – did not, however, increase permissiveness irrespective of the immunocompetence of the mice. Collectively, our work provides detailed insights into RTP4’s role in contributing to HCVs narrow host range and will inform downstream development of a more comprehensive small-animal model for this important disease.
Published in
Receptor transporter protein 4 (RTP4)-mediated repression of hepatitis C virus replication in mouse cells
Schwoerer MP, Carver S, Lin AE et al. · PLoS pathogens 2025 · PMID 40920810 · doi:10.1371/journal.ppat.1013412
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 GSE292032_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 PRJNA1236359 and SRA study SRP570533. Searching any of these in the dataset finder brings you back here.

Study design
16 conditions, mostly with about 6 replicates each
Huh7-Lunet,12h,blank,HCVJc1, ×6 Huh7-Lunet,12h,hsRTP4,HCVJc1, ×6 Huh7-Lunet,12h,mmRTP4,HCVJc1, ×6 Huh7-Lunet,48h,blank,HCVJc1, ×6 Huh7-Lunet,48h,hsRTP4,HCVJc1, ×6 Huh7-Lunet,48h,mmRTP4,HCVJc1, ×6 Huh7-Lunet,72h,hsRTP4,Mock, ×6 Huh7-Lunet,72h,blank,Mock, ×6 +8 more

Supports a between-group comparison across 96 samples.

How we read this: 16 replicated groups read from 96 sample titles; they account for 96 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

+ 56 more — browse all 96 samples with per-sample file links →

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.