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:Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID are debilitating multisystemic conditions sharing similarities in immune dysregulation and cellular signaling pathways contributing to the pathophysiology. In this study, immune exhaustion gene expression was investigated in participants with ME/CFS or long COVID concurrently. RNA was extracted from peripheral blood mononuclear cells isolated from participants with ME/CFS (n = 14), participants with long COVID (n = 15), and healthy controls (n = 18). Participants with ME/CFS were included according to Canadian Consensus Criteria. Participants with long COVID were eligible according to the case definition for "Post COVID-19 Condition" published by the World Health Organization. RNA was analyzed using the NanoString nCounter Immune Exhaustion gene expression panel. Differential gene expression analysis in ME/CFS revealed downregulated IFN signaling and immunoglobulin genes, and this suggested a state of immune suppression. Pathway analysis implicated dysregulated macrophage activation, cytokine production, and immunodeficiency signaling. Long COVID samples exhibited dysregulated expression of genes regarding antigen presentation, cytokine signaling, and immune activation. Differentially expressed genes were associated with antigen presentation, B cell development, macrophage activation, and cytokine signaling. This investigation elucidates the intricate role of both adaptive and innate immune dysregulation underlying ME/CFS and long COVID, emphasizing the potential importance of immune exhaustion in disease progression.
| 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: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:Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disorder with no known underlying mechanisms, diagnostic tools, or treatments. Multiple areas of dysfunction have been extensively studied, but rarely examined together. We recruited age- and sex-matched ME/CFS patients and healthy controls for a multi-modal study examining energy metabolism, immune profiles and plasma protein levels. Adenosine monophosphate (AMP) were higher in immune cells from MECFS patients, with a similar but non-signficant trend observed in plasma. Additionally, immune cells showed higher levels of adenosine diphosphate (ADP) and a reduced adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio. These findings imply decreased ATP generation and the presence of energy stress within the immune cell population. Adaptive immune cell populations were skewed towards less mature effector subsets of CD4+, CD8+ and γδ T cells, and proportions of CD1c+CD141- conventional DC type 2 (cDC2) and CD56lowCD16+ terminal natural killer (NK) cells were also reduced. Elevated levels of plasma proteins associated with thrombus formation and vascular reactivity may contribute to the endothelial dysfunction observed in ME/CFS patients. Using Classification and Regression Tree (CART) modelling, we identified variables from each mode of investigation with strong predictive potential for ME/CFS. Together, this study provides new insights intothe somatic symptoms and underlying biology of ME/CFS.
2025-11-14 | PXD068504 | Pride
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