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Virus Entry is a Major Determinant of HCMV Latency in Monocytes

GSE280650 Homo sapiens (human) RNA-seq (gene expression) 41 samples Submitted 2025/11/27 Platform GPL34281
At a glance

RNA-seq (gene expression) · human · 41 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
41 samples: 11 conditions, mostly in duplicateGroups 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
Viral entry shapes HCMV latency establishmentNature communications · 2025
Summary (written by the submitters)
Human Cytomegalovirus (HCMV) infection can result in either productive or latent infection, the latter being the basis for the virus life-long persistence. Intriguingly, monocytes, which support latent infection, become permissive to productive infection upon differentiation to macrophages. However, the molecular factors explaining these differentiation-driven differences are not fully understood and have been so far attributed to chromatin-mediated repression of the viral genome.
Read the full summary ↓
Here, by using metabolic labeling of newly synthesized RNA early in monocyte and macrophage infection, we discover a major early block in viral gene expression, and viral transcripts are barely detected in infected monocytes. By unbiasedly analyzing the changes between monocytes and their differentiated counterparts, we reveal that the levels of several cell surface proteins involved in HCMV entry are upregulated upon monocyte to macrophage differentiation, and correspondingly we uncover HCMV entry into monocytes compared to macrophages is extremely inefficient. Remarkably, ectopic expression of a canonical HCMV entry receptor in monocytes facilitates productive infection of these cells, demonstrating that given efficient viral entry, monocytes, like macrophages, have the capacity to support productive infection. Among the cell surface proteins that are upregulated upon monocyte differentiation are several integrins, which we show play an important role in HCMV entry into macrophages, partially explaining the differences in viral entry. Overall, our findings reveal that a previously unrecognized major barrier for productive infection in monocytes is entry, adding a critical layer to the paradigm of HCMV latency.
Published in
Viral entry shapes HCMV latency establishment
Kitsberg Y, Nachshon A, Arazi T et al. · Nature communications 2025 · PMID 41457095 · doi:10.1038/s41467-025-68063-y
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 GSE280650_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 PRJNA1179887 and SRA study SRP541997. Searching any of these in the dataset finder brings you back here.

Study design
11 conditions, mostly in duplicate
screen_bright_biorep2 ×5 screen_dim_biorep2 ×5 screen_bright_biorep1 ×3 screen_dim_biorep1 ×3 THP1_monocytes ×2 THP1_macrophages ×2 THP1_PDGFRa ×2 primary_CD14_monocytes ×2 +14 more

Supports a between-group comparison across 30 samples.

How we read this: 11 replicated groups read from 41 sample titles; they account for 30 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

+ 1 more — browse all 41 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.