ArticleJournal of clinical medicine2023
Chronic Fatigue, Depression and Anxiety Symptoms in Long COVID Are Strongly Predicted by Neuroimmune and Neuro-Oxidative Pathways Which Are Caused by the Inflammation during Acute Infection.
Article in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Persistent Redox Imbalance in Post-COVID-19 Syndrome: Lipid Peroxidation, Antioxidant Enzyme Depletion, and Reduced Nitric Oxide Availability in an Amazonian Population.Antioxidants (Basel, Switzerland) · 2026Article
- Unifying the hallmarks of major depression through neuroimmune-metabolic-oxidative (NIMETOX) dysregulation: a mechanistic systems framework.Cellular & molecular immunology · 2026Review
- Comprehensive Immunophenotyping of Monocytes and Dendritic Cells Suggests Distinct Pathophysiology in Chronic Fatigue Syndrome and Long COVID.International journal of molecular sciences · 2026Article
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
- Comparable Immune Alterations and Inflammatory Signatures in ME/CFS and Long COVID.Biomedicines · 2025Article
- Brain-targeted autoimmunity is strongly associated with Long COVID and its chronic fatigue syndrome as well as its affective symptoms.Journal of advanced research · 2025Article
- Neuroimmune, metabolic and oxidative stress pathways in major depressive disorder.Nature reviews. Neurology · 2025Review
- Long COVID-19: A Concept Analysis.Infectious disease reports · 2025Article
- Affective and chronic fatigue symptoms are associated with serum neuronal damage markers in Parkinson's disease.Scientific reports · 2025Article
- Pathogenic Crosstalk Between the Peripheral and Central Nervous System in Rheumatic Diseases: Emerging Evidence and Clinical Implications.International journal of molecular sciences · 2025Review
- Integrating patient and public involvement during the COVID-19 pandemic: lessons from COVID-clinical neuroscience study.Research involvement and engagement · 2025Article
- Persistent immune dysregulation and metabolic alterations following SARS-CoV-2 infection.medRxiv : the preprint server for health sciences · 2025Article
- Observational
- Changes in cerebrovascular reactivity within functional networks in older adults with long-COVID.Frontiers in neurology · 2025Article
- Identifying Factors That Might Affect Outcomes of Exercise-Based Therapies in Long-COVID.Diseases (Basel, Switzerland) · 2024Review
- Long COVID: plasma levels of neurofilament light chain in mild COVID-19 patients with neurocognitive symptoms.Molecular psychiatry · 2024Article
- T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors.Journal of advanced research · 2024Article
- Characterization model of the post COVID-19 condition based on immunological, biochemical, and cytokine markers.iScience · 2024Article
- Differentiation of Prior SARS-CoV-2 Infection and Postacute Sequelae by Standard Clinical Laboratory Measurements in the RECOVER Cohort.Annals of internal medicine · 2024Observational
- Pulmonary redox imbalance drives early fibroproliferative response in moderate/severe coronavirus disease-19 acute respiratory distress syndrome and impacts long-term lung abnormalities.Annals of intensive care · 2024Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong-term coronavirus disease 2019 (long COVID) is associated with physio-somatic (chronic fatigue syndrome and somatic symptoms) and affective (depression and anxiety) symptoms. The severity of the long COVID physio-affective phenome is largely predicted by increased peak body temperature (BT) and lowered oxygen saturation (SpO2) during the acute infectious phase. This study aims to delineate whether the association of BT and SpO2 during the acute phase and the long COVID physio-affective phenome is mediated by neurotoxicity (NT) resulting from activated immune-inflammatory and oxidative stress pathways.
methodsWe recruited 86 patients with long COVID (3-4 months after the acute phase) and 39 healthy controls and assessed serum C-reactive protein (CRP), caspase 1, interleukin (IL) 1β, IL-18, IL-10, myeloperoxidase (MPO), advanced oxidation protein products (AOPPs), total antioxidant capacity (TAC), and calcium (Ca), as well as peak BT and SpO2 during the acute phase.
resultsCluster analysis revealed that a significant part (34.9%) of long COVID patients (n = 30) show a highly elevated NT index as computed based on IL-1β, IL-18, caspase 1, CRP, MPO, and AOPPs. Partial least squares analysis showed that 61.6% of the variance in the physio-affective phenome of long COVID could be explained by the NT index, lowered Ca, and peak BT/SpO2 in the acute phase and prior vaccinations with AstraZeneca or Pfizer. The most important predictors of the physio-affective phenome are Ca, CRP, IL-1β, AOPPs, and MPO.
conclusionThe infection-immune-inflammatory core of acute COVID-19 strongly predicts the development of physio-affective symptoms 3-4 months later, and these effects are partly mediated by neuro-immune and neuro-oxidative pathways.
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