From HHV-6 reactivation to autoimmune reactivity against tight junctions and neuronal antigens, to inflammation, depression, and chronic fatigue syndrome due to Long COVID. DOI
Michaël Maes, Abbas F. Almulla,

Xiaoou Tang

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 30, 2024

Abstract Background Inflammation and autoimmune responses contribute to the pathophysiology of Long COVID, its affective chronic fatigue syndrome (CFS) symptoms, labeled “the physio-affective phenome.” Objectives To investigate whether COVID phenome are linked autoimmunity tight junction proteins, zonulin occludin (ZOOC), immune reactivity lipopolysaccharides (LPS), latter associated with signs human herpes virus-6 reactivation (HHV-6), directed against oligodendrocyte neuronal including myelin basic protein (MBP). Methods IgA / IgM/IgG Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), HHV-6, ZOOC, C-reactive (CRP) advanced oxidation products (AOPP), were measured in 90 patients healthy controls. The was conceptualized as a factor extracted from physical symptom domains. Results Neural network identified LPS (IgA-LPS), IgG-ZOOC, IgG-LPS, IgA-ZOOC most important variables diagnosis an area under ROC curve 0.755. Partial Least Squares analysis showed that 40.9% variance explained by CRP, IgA-MPB IgG-MBP. A large part variances both MBP (36.3-39.7%) (IgA IgG) ZOOC. strongly indicants HHV-6 reactivation, which turn increased IgM-SARS-CoV-2. Conclusions Autoimmunity components junctions bacterial translocation may be involved COVID’s phenome.

Язык: Английский

Abnormal T-Cell Activation And Cytotoxic T-Cell Frequency Discriminates Symptom Severity In Myalgic Encephalomyelitis/Chronic Fatigue Syndrome DOI Open Access
Ji‐Sook Lee, Eliana Lacerda, Caroline C. Kingdon

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Янв. 6, 2025

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating but poorly-understood disease. ME/CFS symptoms can range from mild to severe, and include immune system effects alongside incapacitating post-exertional disease exacerbation. In this study, we examined immunological profiles of people living with by flow cytometry, focusing on cytotoxic cells, determine whether mild/moderate (n= 43) or severe (n=53) expressed different markers. We found that had increased expression effector molecules enhanced proportions early-immunosenescence determined the CD28 - CD57 phenotype, indicative persistent viral infection. contrast, higher activated circulating lymphocytes, CD69 + CD38 expression, more pro-inflammatory cytokines, including IFNγ, TNF IL-17, following stimulation in vitro , prolonged non-specific inflammation. These changes were consistent across cell types CD8 T mucosal associated invariant cells Natural Killer indicating generalised altered responses innate adaptive system. differences likely reflect pathogenesis mechanisms occurring two clinical groups, opening up opportunities for development prognostic markers stratified treatments.

Язык: Английский

Процитировано

0
The Microbiota-Gut-Brain Axis in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Narrative Review of an Emerging Field DOI Creative Commons

Amr Ali Mohamed Abdelgawwad El-Sehrawy,

Ibtihal Ibrahim Ayoub,

Subasini Uthirapathy

и другие.

European Journal of Translational Myology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 12, 2025

The intricate relationship between gut microbiota and the brain has emerged as a pivotal area of research, particularly in understanding myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This complex condition is characterized by debilitating fatigue, cognitive dysfunction, wide array systemic manifestations, posing significant challenges for diagnosis treatment. Recent studies highlight microbiota-gut-brain axis crucial pathway ME/CFS pathophysiology, suggesting that alterations microbial composition may impact immune responses, neurochemical signaling, neuronal health. narrative review systematically explores English-language scholarly articles from January 1995 to 2025, utilizing databases such PubMed, Scopus, Web Science. findings underscore potential targeted therapeutic interventions aimed at correcting dysbiosis. As research progresses, deeper connection could lead innovative approaches managing ME/CFS, ultimately enhancing quality life affected individuals.

Язык: Английский

Процитировано

0
Possible Racial Disparities in the Diagnosis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) DOI Open Access
Chloe Jones, Jarred Younger

International Journal of Environmental Research and Public Health, Год журнала: 2025, Номер 22(2), С. 280 - 280

Опубликована: Фев. 14, 2025

Myalgic encephalomyelitis (ME/CFS) a chronic, disabling illness with no established etiopathology. It has been indicated in some population-based studies that Black and ethnic minority populations are underdiagnosed ME/CFS. The aims of the present study were to (1) identify agreement between receiving an ME/CFS diagnosis meeting diagnostic criteria, (2) demographic characteristics associated diagnosis, (3) explore patient satisfaction healthcare. Self-reported medical history symptoms collected via online survey from respondents without fatigue. self-reporting Center for Disease Control's (CDC) criteria or Institute Medicine (IOM) was assessed Cohen's kappa. Patient predicting physician analyzed logistic regression. Associations demographics, healthcare chi-square tests independence. There 1110 responses. reporting fair (CDC: κ = 0.29; SE 0.02; IOM: 0.28, 0.03). White had 2.94 greater odds being diagnosed than non-White respondents. Having dissatisfaction (χ2 (3, N 1063) 14.17, p 0.003). findings suggest racial disparities processes

Язык: Английский

Процитировано

0
From human herpes virus‐6 reactivation to autoimmune reactivity against tight junctions and neuronal antigens, to inflammation, depression, and chronic fatigue syndrome due to Long COVID DOI Creative Commons
Michael Maes, Abbas F. Almulla,

Xiaoou Tang

и другие.

Journal of Medical Virology, Год журнала: 2024, Номер 96(8)

Опубликована: Авг. 1, 2024

Inflammation and autoimmune responses contribute to the pathophysiology of Long COVID, its affective chronic fatigue syndrome symptoms, labeled "the physio-affective phenome." To investigate whether COVID phenome are linked autoimmunity tight junction proteins, zonulin occludin (ZOOC), immune reactivity lipopolysaccharides (LPS), latter associated with signs human herpes virus-6 (HHV-6) reactivation, directed against oligodendrocyte neuronal including myelin basic protein. IgA/IgM/IgG severe acute respiratory coronavirus 2 (SARS-CoV-2), HHV-6, ZOOC, C-reactive protein (CRP), advanced oxidation products (AOPPs), were measured in 90 patients healthy controls. The was conceptualized as a factor extracted from physical symptom domains. Neural network identified IgA LPS (IgA-LPS), IgG-ZOOC, IgG-LPS, IgA-ZOOC important variables diagnosis an area under ROC curve 0.755. Partial Least Squares analysis showed that 40.9% variance explained by CRP, IgA-myelin (MBP), IgG-MBP. A large part variances both MBP (36.3%-39.7%) (IgA IgG) ZOOC. strongly indicants HHV-6 which turn increased IgM-SARS-CoV-2. Autoimmunity components junctions bacterial translocation may be involved COVID's phenome.

Язык: Английский

Процитировано

3
BioMapAI: Artificial Intelligence Multi-Omics Modeling of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome DOI Creative Commons
Ruoyun Xiong,

Elizabeth Aiken,

Ryan Caldwell

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 28, 2024

Chronic diseases like ME/CFS and long COVID exhibit high heterogeneity with multifactorial etiology progression, complicating diagnosis treatment. To address this, we developed BioMapAI, an explainable Deep Learning framework using the richest longitudinal multi-'omics dataset for to date. This includes gut metagenomics, plasma metabolome, immune profiling, blood labs, clinical symptoms. By connecting asymptom matrix, BioMapAI identified both disease- symptom-specific biomarkers, reconstructed symptoms, achieved state-of-the-art precision in disease classification. We also created first connectivity map of these 'omics healthy states revealed how microbiome-immune-metabolome crosstalk shifted from ME/CFS. Thus, proposed several innovative mechanistic hypotheses ME/CFS: Disrupted microbial functions - SCFA (butyrate), BCAA (amino acid), tryptophan, benzoate lost connection lipids bile acids, activated inflammatory mucosal cells (MAIT, γδT cells) INFγ GzA secretion. These abnormal dynamics are linked key including gastrointestinal issues, fatigue, sleep problems.

Язык: Английский

Процитировано

2
Chronic Fatigue Syndrome: Diagnosis, Treatment, and Future Direction DOI Open Access

B. Sue Graves,

Mitsu Patel,

Hailey Newgent

и другие.

Cureus, Год журнала: 2024, Номер unknown

Опубликована: Окт. 1, 2024

Myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome (CFS), is a complex, condition marked by persistent, debilitating that not alleviated rest and often worsens with physical or mental exertion. Along fatigue, patients experience various symptoms, including cognitive impairments, post-exertional malaise, muscle joint pain, sleep disturbances, immune system dysfunction. Diagnosing CFS/ME challenging due to the absence of definitive biomarkers, overlap symptoms other conditions, lack standardized diagnostic criteria. This comprehensive literature review aims contribute understanding CFS/ME, its diagnosis, pathophysiology, differential treatment, future directions.

Язык: Английский

Процитировано

1
From HHV-6 reactivation to autoimmune reactivity against tight junctions and neuronal antigens, to inflammation, depression, and chronic fatigue syndrome due to Long COVID. DOI
Michaël Maes, Abbas F. Almulla,

Xiaoou Tang

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 30, 2024

Abstract Background Inflammation and autoimmune responses contribute to the pathophysiology of Long COVID, its affective chronic fatigue syndrome (CFS) symptoms, labeled “the physio-affective phenome.” Objectives To investigate whether COVID phenome are linked autoimmunity tight junction proteins, zonulin occludin (ZOOC), immune reactivity lipopolysaccharides (LPS), latter associated with signs human herpes virus-6 reactivation (HHV-6), directed against oligodendrocyte neuronal including myelin basic protein (MBP). Methods IgA / IgM/IgG Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), HHV-6, ZOOC, C-reactive (CRP) advanced oxidation products (AOPP), were measured in 90 patients healthy controls. The was conceptualized as a factor extracted from physical symptom domains. Results Neural network identified LPS (IgA-LPS), IgG-ZOOC, IgG-LPS, IgA-ZOOC most important variables diagnosis an area under ROC curve 0.755. Partial Least Squares analysis showed that 40.9% variance explained by CRP, IgA-MPB IgG-MBP. A large part variances both MBP (36.3-39.7%) (IgA IgG) ZOOC. strongly indicants HHV-6 reactivation, which turn increased IgM-SARS-CoV-2. Conclusions Autoimmunity components junctions bacterial translocation may be involved COVID’s phenome.

Язык: Английский

Процитировано

0