Immune Exhaustion in ME/CFS and long COVID
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ABSTRACT:
PROVIDER: PRJNA1150265 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression analysis of RNA was performed using the commercially available NanoString® nCounter Immune Exhaustion gene expression panel (NanoString Technologies, Seattle, WA, USA). This panel contains 785 genes to elucidate mechanisms behind T cell, B cell and NK cell exhaustion in disease. Ribonucleic acid (RNA) was extracted from peripheral blood mononuclear cells (PBMCs) isolated from ME/CFS (n=14), long COVID (n=15), and healthy control (HC; n=18) participants. ME/CFS participants were included according to Canadian Consensus Criteria for ME. Long COVID participants were eligible according to the working case definition for Post COVID-19 Condition published by the World Health Organization.
2024-11-06 | GSE275334 | GEO
Project description:Long COVID involves activation of proinflammatory and immune exhaustion pathways
| PRJNA939253 | ENA
Project description:Long COVID (LC) involves a spectrum of chronic symptoms after acute severe acute respiratory syndrome coronavirus 2 infection. Current hypotheses for the pathogenesis of LC include persistent virus, tissue damage, autoimmunity, endocrine insufficiency, immune dysfunction and complement activation. We performed immunological, virological, transcriptomic and proteomic analyses from a cohort of 142 individuals between 2020 and 2021, including uninfected controls (n = 35), acutely infected individuals (n = 54), convalescent controls (n = 24) and patients with LC (n = 28). The LC group was characterized by persistent immune activation and proinflammatory responses for more than 180 days after initial infection compared with convalescent controls, including upregulation of JAK-STAT, interleukin-6, complement, metabolism and T cell exhaustion pathways. Similar findings were observed in a second cohort enrolled between 2023 and 2024, including convalescent controls (n = 20) and patients with LC (n = 18). These data suggest that LC is characterized by persistent activation of chronic inflammatory pathways, suggesting new therapeutic targets and potential biomarkers of disease.
2025-10-21 | GSE226260 | GEO
Project description: Not available
| S-EPMC11529985 | biostudies-literature
Project description:We generated reduced representation bisulfite sequencing (RRBS) data of 15 samples (5 Healthy, 5 Long COVID and 5 ME patients) from PBMCs to understand key molecular events involved in Long COVID and ME/CFS.
2025-07-30 | GSE297189 | GEO
Project description:Autoimmunity is an established clinical feature in both Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Post-Acute Sequelae of COVID (PASC). Passive transfer of immunoglobulins from patients' sera into mice induces some clinical features of PASC. IgG-induced transfer of disease phenotypes has long been appreciated, yet the exact mechanism of disease development remains largely elusive. Here, we show that IgG isolated from ME/CFS patients selectively induces mitochondrial fragmentation in primary human endothelial cells and alters mitochondrial energetics. Blocking IgG entry into cells using an Fc blocker inhibits the mitochondrial fragmentation phenotype. Both the digested Fab and Fc regions of IgG separately entered the endothelial cells. However, only the Fab fragment alone was able to alter the mitochondrial energetics, similar to native IgG. Proteomics analysis of IgG-bound immune complex revealed significant and specific changes within the immune complex of ME/CFS and PASC patients compared to healthy controls and other disease controls. We demonstrate that IgGs from ME/CFS patients carry a chronic protective response signal that promotes mitochondrial adaptation to stress through mitochondrial fragmentation, without altering mitochondrial ATP generation capacity in endothelial cells. Our results suggest that chronic and pathogenic IgG-induced mitophagy and metabolic alterations to stress-dependent ATP production may lead to cellular saturation, ultimately affecting mitochondrial health. These results provide an opportunity to develop alternative therapeutic intervention strategies.
2026-02-23 | PXD065439 | Pride
Project description:Background: Women are disproportionately affected by neuropsychiatric symptoms following recovery from acute COVID-19, commonly termed neuropsychiatric long COVID (NP-long COVID). However, whether there are central nervous system-specific changes in gene expression in women with NP-long COVID remains unknown. Methods: Twenty-two women with and ten women without NP-long COVID were enrolled from New Haven, CT, and the surrounding region and consented to a blood draw and large volume lumbar puncture. Total RNA was extracted from cerebrospinal fluid (CSF) cells and peripheral blood mononuclear cells (PBMC). Polyadenylated RNA was then sequenced, and differential expression analyses were performed using DESeq2. Results: Both CSF and PBMC samples showed differential gene expression associated with long COVID status. While some pathways were dysregulated in both the CSF and PBMC of long COVID compared to controls, including those related to androgen response, MTORC1 signaling, and lipid metabolism, these are likely driven by different suites of genes. Moreover, there were also CSF-specific differentially expressed genes in people with long COVID, indicating compartment-specific immune responses. Notably, oxidative stress, reactive oxygen species, and P53 response were all enriched in the CSF of women with long COVID but not PBMC. Conclusions: Women with NP-long COVID show distinct, compartment-specific, transcriptional profiles in the CSF.
2026-01-21 | GSE297499 | GEO
Project description:Recent studies suggest that chronic inflammation and immune dysregulation in the local tissues and systemically play a critical role in the pathophysiology of long COVID. Here, we report a role for nasal epithelium in mediating inflammation in a subset of long COVID patients. We demonstrate impaired barrier function of nasal epithelial cells, inadequate wound healing potential, and nasal cell hypersensitivity along with a persistent inflammatory state in long COVID. These inflamed structural cells activate type 1 innate lymphoid cells in the blood of long COVID patients and propagate systemic inflammation. We demonstrated the importance of understanding the immunological mechanisms driving long COVID to develop effective treatments. We highlight the critical role of the nasal epithelial barrier and the interplay between epithelial cells and ILCs in maintaining mucosal homeostasis and contributing to chronic inflammation in long COVID.
2025-01-31 | GSE286429 | GEO
Project description:CSF immune cell alterations in women with neuropsychiatric Long COVID
| PRJNA1265093 | ENA
Project description:Despite the increasing prevalence of patients with Long Covid Syndrome (LCS), to date the pathophysiology of the disease is still unclear, and therefore diagnosis and therapy are a complex effort without any standardization. To address these issues, we performed a broad exploratory screening study applying state-of-the-art post-genomic profiling methods to blood plasma derived from three groups: 1) healthy individuals vaccinated against SARS-CoV-2 without exposure to the full virus, 2) asymptomatic fully recovered patients at least three months after SARS-CoV-2 infection, 3) symptomatic patients at least 3 months after a SARS-CoV-2 infection, here designated as Long Covid Syndrome (LCS) patients. Multiplex cytokine profiling indicated slightly elevated cytokine levels in recovered individuals in contrast to LCS patients, who displayed lowest levels of cytokines. Label-free proteome profiling corroborated an anti-inflammatory status in LCS characterized by low acute phase protein levels and a uniform down-regulation of macrophagederived secreted proteins, a pattern also characteristic for chronic fatigue syndrome (CFS). Along those lines, eicosanoid and docosanoid analysis revealed high levels of omega-3 fatty acids and a prevalence of anti-inflammatory oxylipins in LCS patients compared to the other study groups. Targeted metabolic profiling indicated low amino acid and triglyceride levels and deregulated acylcarnithines, characteristic for CFS and indicating mitochondrial stress in LCS patients. The anti-inflammatory osmolytes taurine and hypaphorine were significantly up-regulated in LCS patients. In summary, here we present evidence for a specific anti-inflammatory and highly characteristic metabolic signature in LCS which could serve for future diagnostic purposes and help to establish rational therapeutic interventions in these patients.
2023-03-10 | PXD036969 | Pride