The viral origin of myalgic encephalomyelitis/chronic fatigue syndrome

Hanson, Maureen R.

doi:10.1371/journal.ppat.1011523

Cited by 13 publications

(4 citation statements)

References 32 publications

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“…The identification of two leukocytosis episodes preceding health issues, particularly linked to infectious mononucleosis, aligns with the widely accepted understanding of ME/CFS etiology. This observation supports the notion that specific infections, such as herpes viruses, can act as catalysts for ME/CFS development (67)(68)(69)(70). Additionally, recognizing environmental risk factors such as infection, overexertion, toxin exposure and medication side effects as crucial contributors to ME/CFS progression from mild to extremely severe adds significant value.…”

Section: Discussionsupporting

confidence: 78%

Longitudinal cytokine and multi-modal health data of an extremely severe ME/CFS patient with HSD reveals insights into immunopathology, and disease severity

Jahanbani,

Sing,

Maynard

et al. 2024

Front. Immunol.

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IntroductionMyalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) presents substantial challenges in patient care due to its intricate multisystem nature, comorbidities, and global prevalence. The heterogeneity among patient populations, coupled with the absence of FDA-approved diagnostics and therapeutics, further complicates research into disease etiology and patient managment. Integrating longitudinal multi-omics data with clinical, health,textual, pharmaceutical, and nutraceutical data offers a promising avenue to address these complexities, aiding in the identification of underlying causes and providing insights into effective therapeutics and diagnostic strategies.MethodsThis study focused on an exceptionally severe ME/CFS patient with hypermobility spectrum disorder (HSD) during a period of marginal symptom improvements. Longitudinal cytokine profiling was conducted alongside the collection of extensive multi-modal health data to explore the dynamic nature of symptoms, severity, triggers, and modifying factors. Additionally, an updated severity assessment platform and two applications, ME-CFSTrackerApp and LexiTime, were introduced to facilitate real-time symptom tracking and enhance patient-physician/researcher communication, and evaluate response to medical intervention.ResultsLongitudinal cytokine profiling revealed the significance of Th2-type cytokines and highlighted synergistic activities between mast cells and eosinophils, skewing Th1 toward Th2 immune responses in ME/CFS pathogenesis, particularly in cognitive impairment and sensorial intolerance. This suggests a potentially shared underlying mechanism with major ME/CFS comorbidities such as HSD, Mast cell activation syndrome, postural orthostatic tachycardia syndrome (POTS), and small fiber neuropathy. Additionally, the data identified potential roles of BCL6 and TP53 pathways in ME/CFS etiology and emphasized the importance of investigating adverse reactions to medication and supplements and drug interactions in ME/CFS severity and progression.DiscussionOur study advocates for the integration of longitudinal multi-omics with multi-modal health data and artificial intelligence (AI) techniques to better understand ME/CFS and its major comorbidities. These findings highlight the significance of dysregulated Th2-type cytokines in patient stratification and precision medicine strategies. Additionally, our results suggest exploring the use of low-dose drugs with partial agonist activity as a potential avenue for ME/CFS treatment. This comprehensive approach emphasizes the importance of adopting a patient-centered care approach to improve ME/CFS healthcare management, disease severity assessment, and personalized medicine. Overall, these findings contribute to our understanding of ME/CFS and offer avenues for future research and clinical practice.

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Section: Discussionsupporting

confidence: 78%

Longitudinal cytokine and multi-modal health data of an extremely severe ME/CFS patient with HSD reveals insights into immunopathology, and disease severity

Jahanbani,

Sing,

Maynard

et al. 2024

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Traditionally, diagnosing ME/CFS has been challenging, often relying heavily on self-reported questionnaires 74,75 . However, the crux for long-term post- viral infection syndromes like ME/CFS is not necessarily pinpointing an exact diagnosis or tracing disease origins 76,14 (typically infections 77 ), but rather addressing the chronic, multifaceted symptoms that significantly impacts patients’ quality of life 78,79 . Our study introduces a highly nuanced approach to link physiological changes in gut microbiome, plasma metabolome, and immune status, with host symptoms, moving beyond the initial causes of the disease 80,81 .…”

Section: Discussionmentioning

confidence: 99%

BioMapAI: Artificial Intelligence Multi-Omics Modeling of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

Xiong,

Fleming,

Caldwell

et al. 2024

Preprint

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

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“…Enteroviruses and herpesviruses, such as EBV, HHV-6, and CMV, are considered potential etiological factors for viral ME/CFS [ 46 , 205 , 206 ]. Extensive evidence now links ME/CFS to LC [ 222 , 223 , 224 , 225 , 226 , 227 , 228 ].…”

Section: Local Phenomena Of Low-grade Inflammation In Lc and Other Vi...mentioning

confidence: 99%

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement

Gusev,

Sarapultsev

2024

IJMS

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Long COVID (LC), also referred to as Post COVID-19 Condition, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and other terms, represents a complex multisystem disease persisting after the acute phase of COVID-19. Characterized by a myriad of symptoms across different organ systems, LC presents significant diagnostic and management challenges. Central to the disorder is the role of low-grade inflammation, a non-classical inflammatory response that contributes to the chronicity and diversity of symptoms observed. This review explores the pathophysiological underpinnings of LC, emphasizing the importance of low-grade inflammation as a core component. By delineating the pathogenetic relationships and clinical manifestations of LC, this article highlights the necessity for an integrated approach that employs both personalized medicine and standardized protocols aimed at mitigating long-term consequences. The insights gained not only enhance our understanding of LC but also inform the development of therapeutic strategies that could be applicable to other chronic conditions with similar pathophysiological features.

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The viral origin of myalgic encephalomyelitis/chronic fatigue syndrome

Cited by 13 publications

References 32 publications

Longitudinal cytokine and multi-modal health data of an extremely severe ME/CFS patient with HSD reveals insights into immunopathology, and disease severity

Longitudinal cytokine and multi-modal health data of an extremely severe ME/CFS patient with HSD reveals insights into immunopathology, and disease severity

BioMapAI: Artificial Intelligence Multi-Omics Modeling of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement

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