2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T725,Post-COVID-19 syndrome (PCS; also known as post-acute sequelae of COVID-19, PASC and Long COVID) manifests with various clinical symptoms of unclear aetiology that persist or develop months after acute infection with SARS-CoV-2. Potential triggers for PCS include reactivation of latent viruses and autoimmune reactions. In our retrospective cross-sectional and explorative study we compared 48 PCS patients with 48 individuals that recovered fully from COVID-19 (convalescents, CC). We focused on characterising humoral immunity by recording IgG antibody reactivity patterns against Epstein-Barr virus (EBV) EBNA1 antigen using peptide microarray and ELISA methodology as well as determining the presence of autoantibodies. The overall binding landscape of IgG antibodies for the EBV EBNA1 protein was similar for the patients with sequelae versus the convalescents. However, the PCS patients displayed stronger reactivity for epitopes contained within the glycine-alanine repeat region of EBNA1, in particular residues 90-325, and within the central part, amino acids 393-420. Intriguingly, in the latter case, the EBNA1 peptide (residues 405-419) that discriminated the PCS and CC cohorts was localised in a different segment C-terminal from the sequence proposed to be mechanistically associated with multiple sclerosis. The screening for autoantibodies against nuclear/cytoplasmic antigens in HEp-2 cells and against CRYAB, cardiolipin, beta-2-glycoprotein I, IFN-alpha2, IFN-omega, and IL-15 antigens did neither reveal higher prevalence nor increased reactivity in the PCS patients compared to the convalescents. In conclusion, elevated antibody levels against linear peptides derived from residues 90-325 and 405-419 of EBV EBNA1 were the most distinctive characteristics in our cohort of post-COVID-19 syndrome patients.31:T79a,ABSTRACT Post‐COVID‐19 syndrome (PCS; also known as post‐acute sequelae of COVID‐19, PASC and Long COVID) manifests with various clinical symptoms of unclear aetiology that persist or develop months after acute infection with SARS‐CoV‐2. Potential triggers for PCS include reactivation of latent viruses and autoimmune reactions. In our retrospective cross‐sectional and explorative study we compared 48 PCS patients with 48 individuals that recovered fully from COVID‐19 (convalescents, CC). We focused on characterising humoral immunity by recording IgG antibody reactivity patterns against Epstein–Barr virus (EBV) EBNA1 antigen using peptide microarray and ELISA methodology as well as determining the presence of autoantibodies. The overall binding landscape of IgG antibodies for the EBV EBNA1 protein was similar for the patients with sequelae versus the convalescents. However, the PCS patients displayed stronger reactivity for epitopes contained within the glycine–alanine repeat region of EBNA1, in particular residues 90–325, and within the central part, amino acids 393–420. Intriguingly, in the latter case, the EBNA1 peptide (residues 405–419) that discriminated the PCS and CC cohorts was localised in a different segment C‐terminal from the sequence proposed to be mechanistically associated with multiple sclerosis. The screening for autoantibodies against nuclear/cytoplasmic antigens in HEp‐2 cells and against CRYAB, cardiolipin, beta‐2‐glycoprotein I, IFN‐alpha2, IFN‐omega, and IL‐15 antigens did neither reveal higher prevalence nor increased reactivity in the PCS patients compared to the convalescents. In conclusion, elevated antibody levels against linear peptides derived from residues 90–325 and 405–419 of EBV EBNA1 were the most distinctive characteristics in our cohort of post‐COVID‐19 syndrome patients.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Post-COVID-19 Syndrome: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Post-COVID-19 Syndrome (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Post-COVID-19%20Syndrome\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Post-COVID-19 Syndrome\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Post-COVID-19%20Syndrome\"}]}}"}}]],["$","$L2f",null,{"title":"Post-COVID-19 Syndrome: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Post-COVID-19 Syndrome with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1038/s41398-026-04286-x","pmid":"42481444","title":"Understanding neuroinflammation in post-COVID-19 syndrome: biological mechanisms, diagnostic biomarkers, and therapeutic prospects","journal_title":"Translational Psychiatry","journal_issn":"2158-3188","published_at":"2026-07-21T00:00:00.000Z","url":"https://doi.org/10.1038/s41398-026-04286-x","source_score":24,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-24T13:38:11.545Z","updated_at":"2026-07-24T13:38:11.545Z","tags":[{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"category","value":"Psychiatry","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"condition","value":"Cognitive Impairment","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"condition","value":"Neuroinflammation","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"condition","value":"Post-COVID-19 Syndrome","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"modality","value":"Biomarker Assessment","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"modality","value":"Neuroimaging","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"study_design","value":"Expert Review","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"warning","value":"Described as an 'expert review' rather than a systematic review or meta-analysis — no explicit search strategy or inclusion/exclusion criteria are reported in the available text.","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"warning","value":"Full manuscript text was unavailable; summary is based solely on the abstract and publisher page, so specific data, effect sizes, and therapeutic recommendations from the body of the review could not be verified.","value_numeric":null},{"paper_doi":"10.1038/s41398-026-04286-x","tag_type":"warning","value":"Publication date (July 21, 2026) is noted as pre-final-edit ('unedited version'), so content may change before formal indexing.","value_numeric":null}],"summaries":{"what_studied":"This expert review synthesizes current evidence on chronic neuroinflammation as the central driver of post-COVID-19 syndrome (PCS), evaluating fluid and neuroimaging biomarkers and proposing a multiscale longitudinal framework linking immune dysregulation to brain network instability and symptom emergence.","key_result":"Key mechanisms identified include sustained microglial and astrocyte activation, blood-brain barrier disruption, and aberrant cytokine signaling. Fluid biomarkers (GFAP, soluble TREM2, S100β, IL-6, TNF-α) and neuroimaging findings (increased TSPO-PET binding in limbic/frontal regions, altered cerebral blood flow, elevated myo-inositol and choline on MRS, increased free water on diffusion imaging) collectively point to glial activation and network-level dysfunction in PCS.","limitations":"This is a narrative expert review without systematic search methodology or meta-analysis, so findings may reflect selective evidence synthesis. Full manuscript text was not available for review — only the abstract and publisher page were assessed. No primary data or effect sizes are reported.","practice_takeaway":"Clinicians evaluating PCS patients with cognitive or psychiatric complaints should consider neuroinflammation as an underlying mechanism and look for convergent signals across fluid biomarkers (e.g., elevated GFAP, IL-6) and neuroimaging. A multiscale, longitudinal diagnostic approach — rather than reliance on any single biomarker — is recommended to guide future mechanism-based treatments."}},{"doi":"10.1111/sji.70088","pmid":"41518079","title":"Patients Suffering From Post‐\n COVID\n ‐19 Syndrome Feature Enhanced Antibody Reactivity Towards Specific Linear Epitopes Within\n EBV EBNA1","journal_title":"Scandinavian Journal of Immunology","journal_issn":"0300-9475","published_at":"2026-01-10T00:00:00.000Z","url":"https://doi.org/10.1111/sji.70088","source_score":39,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-13","doi":"10.1111/sji.70088","days":"14","issn":"0300-9475","rank":"10","field":"Clinical Medicine","score":"39","category":"Immunology","categories":["Immunology"],"_categories":["Immunology"]},"pubmed":{"doi":"10.1111/sji.70088","title":"Patients Suffering From Post-COVID-19 Syndrome Feature Enhanced Antibody Reactivity Towards Specific Linear Epitopes Within EBV 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Journal of Immunology"],"published-print":{"date-parts":[[2026,1]]},"reference-count":48,"published-online":{"date-time":null,"timestamp":null,"date-parts":[[2026,1,10]]},"references-count":48,"short-container-title":["Scand J Immunol"],"is-referenced-by-count":0},"unpaywall":{"doi":"10.1111/sji.70088","is_oa":true,"title":"Patients Suffering From Post‐\n COVID\n ‐19 Syndrome Feature Enhanced Antibody Reactivity Towards Specific Linear Epitopes Within\n EBV EBNA1","updated":"2026-01-13T16:36:47+00:00","published_date":"2026-01-01","best_oa_location":{"url":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/sji.70088","pmh_id":null,"url_for_pdf":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/sji.70088","url_for_landing_page":"https://doi.org/10.1111/sji.70088"}}},"created_at":"2026-01-16T11:56:46.634Z","updated_at":"2026-01-21T12:05:26.220Z","tags":[{"paper_doi":"10.1111/sji.70088","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"condition","value":"Post-COVID-19 Syndrome","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"sample_size","value":"n=96","value_numeric":96},{"paper_doi":"10.1111/sji.70088","tag_type":"study_design","value":"Cross-Sectional Study","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"warning","value":"No quantitative effect sizes or diagnostic performance metrics are reported in the abstract.","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"warning","value":"Study described as retrospective cross‑sectional and exploratory; design classification is approximate.","value_numeric":null},{"paper_doi":"10.1111/sji.70088","tag_type":"warning","value":"Summary is based on the abstract; full methods and statistical details are not provided.","value_numeric":null}],"summaries":{"what_studied":"Retrospective, cross-sectional, exploratory comparison of 48 patients with post‑COVID‑19 syndrome and 48 fully recovered convalescents, assessing IgG reactivity to EBV EBNA1 by peptide microarray/ELISA and screening select autoantibodies (ANA on HEp‑2; CRYAB, cardiolipin, beta‑2‑glycoprotein I, IFN‑α2, IFN‑ω, IL‑15).","key_result":"PCS patients showed stronger IgG reactivity to EBNA1 epitopes within residues 90–325 (glycine‑alanine repeat) and 393–420; the 405–419 peptide best discriminated PCS from convalescents. Autoantibody screening did not show higher prevalence or increased reactivity in PCS versus convalescents for the tested targets.","limitations":"Retrospective cross‑sectional, exploratory design with a small cohort (48 vs 48). Antibody assessments were limited to EBV EBNA1 epitopes and a narrow autoantibody panel, and no quantitative effect sizes are reported.","practice_takeaway":"In this cohort, PCS was associated with heightened EBNA1 linear epitope IgG responses without broader increases in the tested autoantibodies; this does not support routine autoimmune panels for PCS absent other indications. Clinical utility of EBNA1 epitope testing remains unproven."}}],"initialOffset":2,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Post-COVID-19 Syndrome"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Post-COVID-19 Syndrome"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Post-COVID-19 Syndrome"}}}]]

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