ArticleFrontiers in immunology2023
COVID-19 and trained immunity: the inflammatory burden of long covid.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 19 citations in OpenAlex.
- Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026Review
- Glucagon-like peptide-1 receptor agonist prevents pulmonary fibrosis following acute COVID-19 infection associated with type 2 diabetes.Journal of virology · 2026Article
- Does Timing Matter? Postoperative Risk and the Optimal Timing for Total Joint Arthroplasty Following COVID-19 Infection.Arthroplasty today · 2026Article
- HIV-1 Nef generates lasting innate immune memory in haematopoietic stem and progenitor cells in vivo.EMBO reports · 2026Article
- Trained immunity modulators: A new frontier in immunoregulation and disease intervention.Journal of advanced research · 2026Review
- Comprehensive Immunophenotyping of Monocytes and Dendritic Cells Suggests Distinct Pathophysiology in Chronic Fatigue Syndrome and Long COVID.International journal of molecular sciences · 2026Article
- Discovery of key regulators in classical monocyte phenotypes linked to COVID-19 severity using single-cell multi-omics sequencing.iScience · 2026Article
- How to Employ Trained Immunity and Trained Immunity-Based Vaccines to Inhibit Allergic Inflammation.Vaccines · 2026Review
- Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.Frontiers in immunology · 2026Review
- The "two-hit" storm: a hyper-inflammatory endotype in pediatric long COVID and its role in the severity of secondary bacterial pneumonia-a mechanistic review and clinical implications.Frontiers in public health · 2026Review
- Article
- Review
- COVID-19 Hijacking of the Host Epigenome: Mechanisms, Biomarkers and Long-Term Consequences.International journal of molecular sciences · 2025Review
- Immunological Mechanisms Underlying Allergy Predisposition After SARS-CoV-2 Infection in Children.Cells · 2025Review
- Systems Human Immunology and AI: Immune Setpoint and Immune Health.Annual review of immunology · 2025Review
- Virus-Induced Pathogenic Antibodies: Lessons from Long COVID and Dengue Hemorrhage Fever.International journal of molecular sciences · 2025Review
- Post-pandemic upsurge of group A streptococcus infections: potential link to impaired herd trained immunity following COVID-19 lockdowns.Frontiers in immunology · 2025Article
- Advocating the role of trained immunity in the pathogenesis of ME/CFS: a mini review.Frontiers in immunology · 2025Review
- Amplification of select autonomous HERV loci and surrounding host gene transcription in monocytes from patients with post-acute sequelae of COVID-19.Frontiers in immunology · 2025Article
- Immuno-epigenetic paradigms in coronavirus infection.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe COVID-19 elicits excessive inflammation mediated by innate immune cells like monocytes. Recent evidence reveals extensive epigenetic changes in monocytes during recovery from severe COVID-19, including increased chromatin accessibility at genes related to cytokine production and leukocyte activation. These changes likely originate from the reprogramming of upstream hematopoietic stem and progenitor cells (HSPCs) and represent "trained immunity". HSPC-to-monocyte transmission of epigenetic memory may explain the persistence of these monocyte alterations despite their short lifespan. IL-6 appears pivotal for imprinting durable epigenetic modifications in monocytes during acute infection, with IL-1β potentially playing a contributory role. The poised inflammatory phenotype of monocytes post-COVID-19 may drive chronic inflammation and tissue damage, contributing to post-acute sequelae of COVID-19 symptoms. COVID-19 could also exacerbate inflammation-related diseases, such multisystem inflammatory syndromes, by altering innate immune tendencies via hematopoietic epigenetic reprogramming. Further clinical investigations quantifying inflammatory mediators and mapping epigenetic changes in HSPCs/monocytes of recovering patients are warranted. Research should also examine whether COVID-19 elicits transgenerational inheritance of epigenetic alterations. Elucidating mechanisms underlying COVID-19-induced monocyte reprogramming and developing interventions targeting key inflammatory regulators like IL-6 may mitigate the sustained inflammatory burden imposed by the aberrant trained immunity post-COVID-19.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.