GEO series
Severe long-COVID is driven by monocyte reprogramming and broad immune dysregulation linked to herpesvirus activation
GSE339049
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
48 samples
Submitted 2026/07/22
Platform GPL30173
Summary
Long-COVID (LC) continues to impose a significant burden on patients and society, yet its pathophysiology remains poorly understood. Here, we characterize the functional, transcriptomic, and epigenomic state of monocytes from 21 patients with severe LC (sLC) at a median of 3.4 years after primary infection, as well as the transcriptomic profiles of T and B-cells. Plasma proteomics revealed elevated chemokines and type-I interferon-associated proteins, alongside a reduction in circulating monocytes. Monocytes from sLC patients demonstrated markedly reduced cytokine secretion upon ex vivo LPS stimulation, a finding reproduced in an in vitro model of LC. ATAC-sequencing revealed an epigenomic state of immune dysfunction in monocytes, partially driven by a loss of AP-1 transcription factor binding motifs. Single-cell transcriptomics using STAMP across 113,000 peripheral blood mononuclear cells (PBMCs) confirmed the downregulation of activator protein 1 (AP-1) family members and pro-inflammatory signaling in monocytes, along with impaired antigen presentation, dysregulated viral signaling, and immunosuppressive gene upregulation. T and B-cells demonstrated similar immune dysfunction at the transcriptome level. Epigenomic and transcriptomic evidence of herpesvirus activity, combined with elevated HHV-6 IgG serology in sLC patients, points toward viral reactivation as a candidate mechanism underlying persistent immune dysfunction. Together, these findings suggest that sLC is characterized by a long-lived, infection-induced interferon-priming state that drives monocyte hyporesponsiveness through AP-1-mediated epigenetic reprogramming and implicate HHV-6 reactivation as a potential therapeutic target.
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE339049_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 48 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1496874. Searching any of these in the dataset finder brings you back here.
Study design
40 conditions, each sampled once — no replicated groups
Read from the first 40 of 48 sample titles: 40 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
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- GSM9887629 IM06_Mild
- GSM9887630 IM07_Nonsymptomatic
- GSM9887631 IM08_Mild
- GSM9887632 IM09_Mild
- GSM9887633 IM10_Nonsymptomatic
- GSM9887634 IM11_Mild
- GSM9887635 IM12_Nonsymptomatic
- GSM9887636 IM13_Nonsymptomatic
- GSM9887637 IM14_Mild
- GSM9887638 IM15_Nonsymptomatic
- GSM9887639 IM16_Nonsymptomatic
- GSM9887640 IM17_Nonsymptomatic
- GSM9887641 IM18_Nonsymptomatic
- GSM9887642 IM19_Nonsymptomatic
- GSM9887643 IM20_Mild
- GSM9887644 IM21_Mild
- GSM9887645 IM22_Mild
- GSM9887646 IM23_Nonsymptomatic
- GSM9887647 IM24_Mild
- GSM9887648 IM29_Nonsymptomatic
- GSM9887649 IM30_Nonsymptomatic
- GSM9887650 IM31_Mild
- GSM9887651 IM33_Mild
- GSM9887652 IM34_Nonsymptomatic
- GSM9887653 IM35_Nonsymptomatic
- GSM9887654 IM37_Nonsymptomatic
- GSM9887655 IM38_Mild
- GSM9887656 IM39_Mild
- GSM9887657 IM40_Nonsymptomatic
- GSM9887658 IM41_Nonsymptomatic
- GSM9887659 IM43_Severe
- GSM9887660 IM44_Severe
- GSM9887661 IM45_Severe
- GSM9887662 IM46_Severe
- GSM9887663 IM47_Severe
- GSM9887664 IM48_Severe
- GSM9887665 IM49_Severe
- GSM9887666 IM50_Severe
- GSM9887667 IM51_Severe
- GSM9887668 IM53_Severe
+ 8 more — browse all 48 samples with per-sample file links →
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