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:T916, Aim This study investigated coronary slow flow (CSF) prevalence in post-COVID-19 patients presenting with unstable angina (UA) and angiographically normal coronary arteries. Materials and methods The study included 190 patients presenting with unstable angina (UA) and confirmed normal coronary arteries via invasive angiography. Participants were divided into two age- and sex-matched groups: 95 patients with a history of COVID-19 [COVID (+) UA-NCA] and 95 patients without a prior history of the infection [COVID (–) UA-NCA]. In the study group, COVID-19 was confirmed via RT-PCR and computed tomography. All participants underwent coronary angiography to perform Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) measurements. CSF was diagnosed in patients with a corrected TFC (CTFC) ≥ 27. Results CSF prevalence was significantly higher in the COVID (+) UA-NCA group than in the COVID (–) UA-NCA group (18.9% vs. 5.3%, p = 0.003). Individual CTFC values for the LAD, LCX, and RCA were also significantly higher in the COVID (+) UA-NCA group compared to the COVID (–) UA-NCA group (26.1 ± 4.3 vs. 22.4 ± 2.6 [ p = 0.01], 24.3 ± 4.5 vs. 21.7 ± 2.4 [ p < 0.001], and 24.3 ± 4.5 vs. 21.4 ± 2.5 [ p < 0.001], respectively). Conclusions CSF prevalence is significantly higher in patients with a history of COVID-19, suggesting persistent microvascular impairment. 31:T76c,Post-viral syndromes are heterogeneous multisystem diseases without a uniform etiology that occur as a result of acute viral infections. During the COVID-19 pandemic, the number of patients increased dramatically due to infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This is known as post-acute sequelae of COVID-19 (PASC), with many cases also meeting the criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), the most severe form of a post-viral disease, characterized by severe fatigue, post-exertional malaise (PEM), unrefreshing sleep, neurocognitive impairment, and autonomic and immune dysregulation. Orexin (OX) neuropeptides, which regulate arousal, metabolism, and neuroendocrine functions, may serve as a central link between stress, immune activation, and metabolic changes in these syndromes. Notable phenotypic similarities between OX system dysfunction and core features of PASC and ME/CFS, including fatigue, sleep issues, impaired glucose metabolism, and neuropsychiatric symptoms, support a mechanistic model in which impaired OX signaling contributes to post-viral endocrine and metabolic dysfunction. This review examines the role of OX in regulating glucose metabolism, HPA axis activity, and systemic homeostasis, with a specific focus on sexually dimorphic expression and function in relation to post-viral syndromes. We also highlight the effect of glucagon-like peptide-1 (GLP-1), another key player in metabolism, which also has neuroprotective, anti-inflammatory, vasoprotective, and immunomodulatory effects. We further emphasize emerging therapeutic strategies, such as GLP-1 receptor agonists (GLP-1RAs) and drugs targeting the OX system. Together, these insights provide an integrated framework for understanding and targeting the neuroendocrine-metabolic underpinnings of PASC, ME/CFS, and other post-viral syndromes.32:T7cb,Abstract Postviral syndromes are heterogeneous multisystem diseases without a uniform etiology that occur as a result of acute viral infections. During the COVID-19 pandemic, the number of patients increased dramatically due to infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This is known as postacute sequelae of COVID-19 (PASC), with many cases also meeting the criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), the most severe form of a postviral disease, characterized by severe fatigue, postexertional malaise (PEM), unrefreshing sleep, neurocognitive impairment, and autonomic and immune dysregulation. Orexin (OX) neuropeptides, which regulate arousal, metabolism, and neuroendocrine functions, may serve as a central link among stress, immune activation, and metabolic changes in these syndromes. Notable phenotypic similarities between OX system dysfunction and core features of PASC and ME/CFS, including fatigue, sleep issues, impaired glucose metabolism, and neuropsychiatric symptoms, support a mechanistic model in which impaired OX signaling contributes to postviral endocrine and metabolic dysfunction. This review examines the role of OX in regulating glucose metabolism, HPA axis activity, and systemic homeostasis, with a specific focus on sexually dimorphic expression and function in relation to postviral syndromes. We also highlight the effect of glucagon-like peptide-1 (GLP-1), another key player in metabolism, which also has neuroprotective, anti-inflammatory, vasoprotective, and immunomodulatory effects. We further emphasize emerging therapeutic strategies, such as GLP-1 receptor agonists (GLP-1RAs) and drugs targeting the OX system. Together, these insights provide an integrated framework for understanding and targeting the neuroendocrine-metabolic underpinnings of PASC, ME/CFS, and other postviral syndromes.33:T6e1,Increasing evidence suggests that reactivation of latent EBV in patients with COVID-19 may be linked to the development of post-acute sequelae of COVID-19, colloquially known as Long COVID. However, the reason for this co-occurrence of primary infection and reactivation of latent viruses remains elusive. During the first wave of COVID-19, we assessed all major immune cell populations by flow cytometry in a cohort of 61 patients with moderate to critical COVID-19 at the time of hospitalization. Additional blood samples from these patients were biobanked for later analysis. Using these biobanked samples, we evaluated the co-occurrence of CMV, EBV, as well as HHV-6A and -6B by qPCR. EBV was found to be reactivated not only in patients with critical or severe COVID-19 (24/33 patients; 72.72%), but also in patients with moderate COVID-19 disease (19/28; 67.86%) at the time of hospital admission. In contrast, HHV-6A was not detected among any patients, whereas CMV and HHV-6B only occurred in low frewuencies (7.1–12.1% and 10.7–15.2%, respectively). In COVID-19 patients with EBV reactivation, the degree of expression of the T-cell co-stimulatory CD28 and co-expression of CD28 and the integrin CD11a was diminished on CD8 T-cells. In contrast, the frequency of CD8 T-cells expressing the proliferative exhaustion marker CD57 increased. Collectively, these data point to an altered activation phenotype of circulating CD8 T cells and that higher replicative senescence is associated with EBV reactivation. The data presented here suggests an alteration in the CD8 T-cell compartment with impaired ability to control the EBV reactivation in COVID patients. The online version contains supplementary material available at 10.1007/s00430-026-00873-3.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Post-Acute Sequelae of COVID-19: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Post-Acute Sequelae of COVID-19 (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Post-Acute%20Sequelae%20of%20COVID-19\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Post-Acute Sequelae of COVID-19\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Post-Acute%20Sequelae%20of%20COVID-19\"}]}}"}}]],["$","$L2f",null,{"title":"Post-Acute Sequelae of COVID-19: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Post-Acute Sequelae of COVID-19 with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1007/s00246-026-04424-8","pmid":"42635737","title":"Cardiovascular Sequelae After SARS-CoV-2 in Children: From Myocardial Injury to Dysautonomia and Implications for Phenotype-Guided Follow-Up","journal_title":"Pediatric Cardiology","journal_issn":"0172-0643","published_at":"2026-08-24T00:00:00.000Z","url":"https://doi.org/10.1007/s00246-026-04424-8","source_score":18,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-28T06:25:15.113Z","updated_at":"2026-08-28T06:25:15.113Z","tags":[{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"age_group","value":"pediatric","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"category","value":"Pediatrics","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"condition","value":"Autonomic Dysfunction","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"condition","value":"Multisystem Inflammatory Syndrome in Children","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"condition","value":"Myocarditis","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"condition","value":"Post-Acute Sequelae of COVID-19","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"condition","value":"Postural Orthostatic Tachycardia Syndrome","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"warning","value":"Multiple MUSIC study publications (echocardiography, strain, CMR) share overlapping patient populations and were not treated as independent cohorts in this review.","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"warning","value":"Several prevalence figures for residual GLS and CMR abnormalities come from small, selected cohorts enriched for severe disease or specialist referral, likely overestimating true rates.","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"warning","value":"The autonomic dysfunction cohorts (e.g., POTS prevalence of 62.5%) were drawn from specialist rehabilitation or syncope clinics, not general post-COVID populations.","value_numeric":null},{"paper_doi":"10.1007/s00246-026-04424-8","tag_type":"warning","value":"This is a narrative (not systematic) review; quantitative pooling was not performed due to study heterogeneity, so prevalence figures cited are from individual cohorts and should not be interpreted as population estimates.","value_numeric":null}],"summaries":{"what_studied":"Narrative review of paediatric cardiovascular sequelae after SARS-CoV-2, covering MIS-C, subclinical myocardial dysfunction (GLS, CMR), and autonomic dysfunction in children; literature search January 2020 – May 2026, minimum 4-week follow-up required for inclusion.","key_result":"Overt cardiac dysfunction after MIS-C resolved in the vast majority of children across cohorts (e.g., 98.3% in a Krakow cohort; all but one patient in the MUSIC cohort by 6 months). However, persistent GLS impairment was reported in 13–35.7% of selected cohorts at 6–12 months, and residual LGE on CMR in up to 33% of smaller studies, though the large MUSIC CMR analysis found only 3.5% met Lake Louise criteria at follow-up. Autonomic dysfunction (including POTS in 62.5% of one small retrospective cohort) contributed to persistent symptoms when conventional cardiac evaluation was normal.","limitations":"- Substantial heterogeneity in case definitions, follow-up timing, and diagnostic protocols prevents pooled estimates.\n- Most studies are single-centre with small samples; CMR and CPET often performed only in selected subgroups, introducing referral bias.\n- Long-term prognostic significance of isolated GLS or CMR abnormalities is unknown; no validated discharge criteria exist.","practice_takeaway":"Reserve ongoing cardiology surveillance for children with persistent objective cardiac abnormalities (ventricular dysfunction, arrhythmia, coronary aneurysm, elevated biomarkers); asymptomatic children with normal ECG, echo, and biomarkers at 4–6 weeks can be discharged from routine follow-up. Children with palpitations, orthostatic symptoms, or fatigue but normal conventional cardiac studies should be redirected to autonomic evaluation and rehabilitation rather than escalating cardiac imaging."}},{"doi":"10.1007/s10067-026-08302-9","pmid":"42461564","title":"Association of oral outpatient antiviral medications for COVID-19 with the risk of post-acute sequelae of COVID-19 at 28 and 90 days in a cohort of individuals with systemic autoimmune rheumatic diseases","journal_title":"Clinical Rheumatology","journal_issn":"0770-3198","published_at":"2026-07-16T00:00:00.000Z","url":"https://doi.org/10.1007/s10067-026-08302-9","source_score":3,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-25T13:57:43.299Z","updated_at":"2026-07-25T13:57:43.299Z","tags":[{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"brand","value":"Paxlovid","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"condition","value":"Inflammatory Arthritis","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"condition","value":"Post-Acute Sequelae of COVID-19","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"condition","value":"Systemic Autoimmune Rheumatic Disease","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"generic","value":"molnupiravir","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"generic","value":"nirmatrelvir/ritonavir","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"modality","value":"Antiviral","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"sample_size","value":"n=431","value_numeric":431},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"warning","value":"Antiviral assignment was not randomized; confounding by indication (e.g., higher-risk patients more likely prescribed antivirals) may bias results in either direction.","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"warning","value":"Molnupiravir and nirmatrelvir/ritonavir were analyzed together as a single 'antiviral' group, which may obscure differential effects between the two agents.","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08302-9","tag_type":"warning","value":"The 90-day PASC result (aOR 0.44) is numerically promising but statistically non-significant — should not be interpreted as confirmed benefit.","value_numeric":null}],"summaries":{"practice_takeaway":"For patients with rheumatic diseases, oral COVID-19 antivirals do not clearly prevent long COVID at 28 days, but may reduce 90-day PASC risk — a finding to weigh alongside established benefits for acute disease severity. Clinicians should continue standard antiviral prescribing decisions while awaiting more definitive data in this population.","what_studied":"This prospective cohort study examined whether oral outpatient antivirals (nirmatrelvir/ritonavir or molnupiravir) reduced the risk of PASC (long COVID) at 28 and 90 days in 431 adults with systemic autoimmune rheumatic diseases (SARDs) at Mass General Brigham, from December 2021 to January 2025.","key_result":"Antiviral use showed no difference in PASC at 28 days (30.9% vs. 31.1%; aOR 0.98, 95% CI 0.64–1.49) but was associated with numerically lower odds at 90 days (5.2% vs. 10.5%; aOR 0.44, 95% CI 0.19–1.02), with the confidence interval crossing 1.","limitations":"- The 90-day result did not reach statistical significance (CI crosses 1.0), limiting firm conclusions.\n- Single health system cohort (Mass General Brigham), predominantly female (81%) and highly vaccinated (96%), limiting generalizability.\n- Observational design with potential for residual confounding by indication (sicker patients may have been more likely to receive antivirals)."}},{"doi":"10.3389/fcvm.2026.1814606","pmid":null,"title":"Impact of COVID-19 history on the prevalence of coronary slow flow: a comparative study in unstable angina patients","journal_title":"Frontiers in Cardiovascular Medicine","journal_issn":"2297-055X","published_at":"2026-05-08T00:00:00.000Z","url":"https://doi.org/10.3389/fcvm.2026.1814606","source_score":106,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-11","doi":"10.3389/fcvm.2026.1814606","days":"7","issn":"2297-055X","rank":"4","field":"Clinical Medicine","score":"106","category":"Cardiac & Cardiovascular Systems","categories":["Cardiac & Cardiovascular Systems"],"_categories":["Cardiac & Cardiovascular 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CTFC values were significantly higher across all three major vessels (LAD: 26.1 vs. 22.4, p = 0.01; LCX: 24.3 vs. 21.7, p < 0.001; RCA: 24.3 vs. 21.4, p < 0.001). On multivariate analysis, COVID-19 history was the only independent predictor of CSF (Beta = 0.214, p = 0.005).","limitations":"- Retrospective single-center design limits generalizability.\n- No inflammatory biomarkers measured at the time of angiography.\n- COVID-19 vaccination status and initial infection severity were not recorded, potentially confounding the degree of persistent endothelial dysfunction.","practice_takeaway":"Clinicians should maintain a high index of suspicion for coronary microvascular dysfunction in post-COVID-19 patients presenting with unstable angina and clean coronaries — CSF was nearly 4 times more common up to 6 months after infection. 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EBV reactivation was linked to decreased CD28 expression on CD8 T-cells (p=0.013), decreased CD11a++CD28+CD57− CD8 T-cells (p=0.0036), and increased CD28−CD11a−CD57+ CD8 T-cells (p=0.0024), indicating a senescent, exhausted phenotype. CMV and HHV-6B were detected in only 7–12% and 11–15% of patients, respectively; HHV-6A was absent.","limitations":"- Cross-sectional design prevents determining whether EBV reactivation causes or results from CD8 T-cell changes, and cannot link findings to PASC outcomes (majority lost to follow-up).\n- Serological status against herpesviruses was not assessed, so subclinical or low-level reactivation may be underestimated.\n- Small single-region cohort (n=61) limits generalizability; p-values were not corrected for multiple comparisons.","practice_takeaway":"EBV reactivation is common across all severities of hospitalized COVID-19, not just critical cases, and is tied to CD8 T-cell exhaustion markers. Clinicians evaluating Long COVID patients should consider EBV reactivation as part of the immune dysregulation picture, though its direct causal role in PASC remains unproven."}}],"initialOffset":5,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Post-Acute Sequelae of COVID-19"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Post-Acute Sequelae of COVID-19"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Post-Acute Sequelae of COVID-19"}}}]]

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