Hypocortisolemic ASIA: a vaccine- and chronic infection-induced syndrome behind the origin of long COVID and myalgic encephalomyelitis DOI Creative Commons
Manuel Ruiz-Pablos, Bruno Paiva, Aintzane Zabaleta

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: July 9, 2024

Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS), long COVID (LC) and post-COVID-19 vaccine show similarities in their pathophysiology clinical manifestations. These disorders are related to viral adjuvant persistence, immunological alterations, autoimmune diseases hormonal imbalances. A developmental model is postulated that involves the interaction between immune hyperactivation, hypophysitis pituitary hypophysitis, depletion. This process might begin with a deficient CD4 T-cell response infections genetically predisposed individuals (HLA-DRB1), followed by an uncontrolled CD8 hyperactivation elevated antibody production, some of which may be directed against autoantigens, can trigger direct damage pituitary, resulting decreased production hormones, such as ACTH. As disease progresses, prolonged exposure antigens lead exhaustion system, exacerbating symptoms pathology. It suggested these could included autoimmune/adjuvant-induced inflammatory (ASIA) because similar manifestations possible relationship genetic factors, polymorphisms HLA-DRB1 gene. In addition, it proposed treatment antivirals, corticosteroids/ginseng, antioxidants, metabolic precursors improve modulating response, function, inflammation oxidative stress. Therefore, purpose this review suggest origin adenohypophysis improvement after corticosteroid replacement therapy.

Language: Английский

Immunothrombotic involvement in COVID-19 DOI
José A. Páramo, María Marcos‐Jubilar

Elsevier eBooks, Journal Year: 2025, Volume and Issue: unknown, P. 335 - 352

Published: Jan. 1, 2025

Language: Английский

Citations

0
Tryptophan metabolism reprogramming contributes to the prothrombotic milieu in mice and humans infected with SARS-CoV-2 DOI Open Access
Saravanan Subramaniam, Marc A. Napoleon, Saran Lotfollahzadeh

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 21, 2025

SARS-CoV-2 infection disturbs the coagulation balance in blood, triggering thrombosis and contributing to organ failure. The role of prothrombotic metabolites COVID-19-associated coagulopathy remains elusive. Leveraging K18-hACE2 mice infected with SARS-CoV-2, we observed higher levels tryptophan metabolite, kynurenine, compared controls. SARS CoV-2 showed a significant upregulation enzymes controlling Kynurenine biogenesis, such as indoleamine 2,3-dioxygenase (IDO-1) kidneys liver, respectively, well changes involved kynurenine catabolism, including monooxygenase kynurinase. Consistent agonistic these Aryl Hydrocarbon Receptor (AHR) signaling, AHR activation its downstream mediator, tissue factor (TF), highly potent procoagulant factor, was endothelial cells (ECs) lungs mice. These findings were validated humans, where controls, sera COVID-19 patients increased Kynurenine, kynurenic acid, anthranilic quinolinic acid. Activation AHR-TF axis noted patients, IDO-1 activity than Levels Kyn correlated strongly TF inducing on ECs. A specific inhibitor or separately combination suppressed sera-induced Together, identified upregulated by infection, resulting augmented catabolites, thereby suggesting possibly new diagnostic and/or therapeutic target.

Language: Английский

Citations

0
Exploring Prognostic Markers for Patients With COVID‐19 in a Low‐Resource Setting: A Cross‐Sectional Study DOI Creative Commons
Md Asaduzzaman,

Mohammad Romel Bhuia,

Mohammad Zabed Jillul Bari

et al.

International Journal of Clinical Practice, Journal Year: 2025, Volume and Issue: 2025(1)

Published: Jan. 1, 2025

Aim: Triaging patients based on prognostic biomarkers may contribute to better management of at‐risk in resource‐constrained settings. This study aimed explore readily available and cost‐effective predictors mortality among COVID‐19 patients. Methods: cross‐sectional study, conducted across multiple centers, involved with admitted four hospitals Bangladesh. The analysis encompassed demographic information, clinical features, laboratory findings, in‐hospital outcomes. Logistic regression was utilized identify factors contributing risk. Results: Among 442 patients, 55 (12.44%) experienced mortality. patients’ mean 60 ± 14 years. DM (76% vs. 62%), IHD (42% 19%), CKD (35% 15%), COPD (24% 11%) were the most prevalent comorbidities nonsurvivors. Compared survivor group, median NLR (7 4.1; p = 0.005), ferritin (507 328; 0.21), D‐dimer (900 567; 0.12) higher nonsurvivor group. Higher age (OR 1.05; 95% CI 1.02–1.08), coexisting 2.59; 1.27–5.29), leukocytosis 2.52; 1.21–5.28), thrombocytopenia 0.27; 0.12–0.61), lower SpO2 upon admission 0.92; 0.89–0.95), more extensive lung involvement CT 1.01; 1.001–1.03) significant risk death.

Language: Английский

Citations

0
Infection in Childhood Arterial Ischemic Stroke: Metagenomic Next-Generation Sequencing Results of the VIPS II Study DOI
Mary Rolfes, Prashanth Ramachandran, Anne E. Wapniarski

et al.

Stroke, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Acute respiratory infection transiently increases risk for childhood arterial ischemic stroke (AIS). We hypothesize that this paradox of a common exposure linked to rare outcome could be explained by either (1) the hypothesis: unusual or multiple pathogens (2) host response heterogeneity in inflammatory infection. leverage metagenomic next-generation sequencing (mNGS), comprehensive microbial detection tool, test first hypothesis. The VIPS II study (Vascular Effects Infection Pediatric Stroke II) prospectively enrolled children with AIS at 22 international sites over 5 years (December 2016 January 2022). Sites measured prestroke clinical via standardized parental interviews and chart abstraction. To assess more broadly background spectrum pathogens, central research laboratory performed mNGS on plasma oropharyngeal swabs collected within 72 hours stroke. was also biological samples from stroke-free (June 2017 2022), both without (well) (ill) documentation 205 patients AIS, 95 well children, 47 ill children. Clinical infection, most commonly upper tract detected 81 (40%) patients. Both swab data were available 190 91 27 viruses (14%) 9 (10%), (33%) Most viruses. Coinfections rare. Similar found variety suggesting type does not explain susceptibility. Rather, alternative hypothesis regarding an immune infections pathogenicity should further explored.

Language: Английский

Citations

0
Predictive value of inflammatory and coagulation biomarkers for venous thromboembolism in COVID-19 patients DOI Open Access

Marta Hojker,

Jure Tršan,

Uroš Tršan

et al.

Clinical Hemorheology and Microcirculation, Journal Year: 2023, Volume and Issue: 83(4), P. 387 - 395

Published: Jan. 20, 2023

The predictive value of coagulation markers for venous thromboembolism (VTE) in COVID-19 patients has been investigated with conflicting results.Our aim was to investigate the correlation between biomarkers and VTE D-dimer hospitalized patients.Complete blood count, inflammatory at admission were collected. defined as diagnosed pulmonary embolism or deep vein thrombosis. Events in-hospital death ICU admission. Predictors identified Pearson prediction models. A ROC curve constructed assess D-dimer.1651 participants included, 111 identified. incidence higher group (49.5% vs 28.2%, p < 0.001). Neutrophil-lymphocyte ratio (NLR, 0.001; 95% CI 0.000-0.002; 0.019) (0.00005; 0.00002-0.00008; 0.001), Geneva score (0.026; 0.012-0.040; 0.001) Wells (0.047; 0.033-0.061; associated VTE. had a goor (ROC area 0.85, 0.816-0.893), an optimal cut-off 2677μg/L (Youden index 0,602).Among best VTE, but values should be used COVID-19.

Language: Английский

Citations

8
Long COVID and Wavering Incidence of Pulmonary Embolism: A Systematic Review DOI Creative Commons
Bushra Shah,

Mah Noor Ahmad,

Musfira Khalid

et al.

Journal of Community Hospital Internal Medicine Perspectives, Journal Year: 2023, Volume and Issue: 13(5)

Published: Sept. 2, 2023

Pulmonary embolism (PE) is a serious medical condition that can occur as result of venous thromboembolism (VTE). COVID-19, also known Post-Acute Sequelae SARS-CoV-2 infection (PASC), potentially lead to PE due the formation blood clots in lungs. This study aims collate and report trends patients with long COVID (4-12 weeks since infection) post-COVID-19 syndrome (>12 infection). The adhered PRISMA Statement 2020 guidelines, systematic search was conducted four databases. In total, nine observational studies were included total patient count 45,825,187. incidence COVID/post-COVID-19 seen among 31,885 individuals out 44,967,887 participants. rate observed 0.07%, given matched controls. While we cannot state certainty COVID-19 itself leads higher risks at later time, this emphasizes need for optimized care longitudinal during era account deviations from norm.

Language: Английский

Citations

8
Viral Infection and Ischemic Stroke: Emerging Trends and Mechanistic Insights DOI Creative Commons

Michael Clarke,

Sarina Falcione, Roobina Boghozian

et al.

Journal of the American Heart Association, Journal Year: 2024, Volume and Issue: 13(18)

Published: Sept. 11, 2024

Population studies have suggested that viral infections may be contributing to risk of ischemic stroke, although the mechanisms for this are unclear. In review, we examine epidemiological evidence supporting involvement diseases, including influenza, COVID‐19, chronic herpesvirus infections, and hepatitis C in current trends stroke incidence. To support these associations, highlight virus–host interactions critical context direct effects acute persistent on vascular function, inflammation, thrombosis. Additionally, evaluate systemic changes occur during infection can predispose individuals alterations blood pressure regulation, coagulation, lipid metabolism. Our review emphasizes need further elucidate precise involved risk. Future research will inform development targeted interventions prevention diseases.

Language: Английский

Citations

3
Vascular Function, Systemic Inflammation, and Coagulation Activation 18 Months after COVID-19 Infection: An Observational Cohort Study DOI Open Access
Loes H. Willems, Lotte M. C. Jacobs, Laszlo Groh

et al.

Journal of Clinical Medicine, Journal Year: 2023, Volume and Issue: 12(4), P. 1413 - 1413

Published: Feb. 10, 2023

Introduction: Among its effect on virtually all other organs, COVID-19 affects the cardiovascular system, potentially jeopardizing health of millions. Previous research has shown no indication macrovascular dysfunction as reflected by carotid artery reactivity, but sustained microvascular dysfunction, systemic inflammation, and coagulation activation at 3 months after acute COVID-19. The long-term effects vascular function remain unknown. Materials Methods: This cohort study involved 167 patients who participated in COVAS trial. At 18 COVID-19, was evaluated measuring diameter response to cold pressor testing. Additionally, plasma endothelin-1, von Willebrand factor, Interleukin(IL)-1ra, IL-6, IL-18, factor complexes were measured using ELISA techniques. Results: prevalence did not differ between (14.5%) (11.7%) infection (p = 0.585). However, there a significant decrease absolute change, 3.5% ± 4.7 vs. 2.7% 2.5, p—0.001, respectively. levels vWF:Ag persistently high 80% survivors, reflecting endothelial cell damage possibly attenuated function. Furthermore, while inflammatory cytokines interleukin(IL)-1RA IL-18 normalized evidence contact pathway longer present, concentrations IL-6 thrombin:antithrombin further increased versus (2.5 pg/mL 2.6 4.0 4.6, p 0.006 4.9 μg/L 4.4 18.2 11.4, < 0.001, respectively). Discussion: shows that infection, incidence defined constrictive during reactivity testing is increased. Nonetheless, biomarkers indicate (vWF), inflammation (IL-6), extrinsic/common (FVII:AT, TAT) infection.

Language: Английский

Citations

7
Proteomics of serum-derived extracellular vesicles are associated with the severity and different clinical profiles of patients with COVID-19: An exploratory secondary analysis DOI
Adriana Franco Paes Leme, Sami Yokoo, Ana Gabriela Costa Normando

et al.

Cytotherapy, Journal Year: 2024, Volume and Issue: 26(5), P. 444 - 455

Published: Feb. 15, 2024

Language: Английский

Citations

2
Aging is associated with an insufficient early inflammatory response of lung endothelial cells in SARS-CoV-2 infection DOI Creative Commons
Saravanan Subramaniam, Devin Kenney,

Archana Jayaraman

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: June 7, 2024

Advanced age is associated with an increased susceptibility to Coronavirus Disease (COVID)-19 and more severe outcomes, although the underlying mechanisms are understudied. The lung endothelium located next infected epithelial cells bystander inflammation may contribute thromboinflammation COVID-19-associated coagulopathy. Here, we investigated age-associated SARS-CoV-2 pathogenesis endothelial inflammatory responses using humanized K18-hACE2 mice. Survival was reduced 20% in aged mice (85–112 weeks) versus 50% young (12–15 at 10 days post infection (dpi). Bulk RNA-sequencing of from mock 2dpi both groups (aged: 72–85 weeks; young: 15 showed substantially lower significant differentially regulated genes than (712 2294 genes). Viral recognition anti-viral pathways such as RIG-I-like receptor signaling, NOD-like signaling interferon were response SARS-CoV-2. Young several fold higher ( Ifitm3 , Ifit1 Isg15, Stat1 ) interferon-induced chemokines Cxcl10 Cxcl11 Endothelial displayed elevated expression Cxcl9 Ccl2 leukocyte adhesion markers Icam1 underscoring that during could facilitate thromboinflammation. TREM1 acute phase particularly prominent Immunohistochemistry unable detect viral protein pulmonary endothelium. In conclusion, our data demonstrate early host declines aging, which be a potential contributor disease severity.

Language: Английский

Citations

2