Genetics of <scp>COVID</scp>‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Tziastoudi, Maria; Cholevas, Christos; Stefanidis, Ioannis; Theoharides, Theoharis C.

doi:10.1002/acn3.51631

Cited by 4 publications

(3 citation statements)

References 288 publications

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“…The most significant gene alterations in ME/CFS have been summarized by Deumer et al [71] and indicate pathways related to immunity, inflammation, neurotransmission, oxidative stress, the catecholamine pathway, the serotoninergic system, and circadian rhythm. A systematic review by Tziastoudi et al [72] on gene alterations-common in ME/CFS and long COVID-highlighted the involve-ment of genes related to inflammation (mediated by chemokine-and cytokine-signaling pathways), T-cell activation, and Toll-like receptor-signaling pathways.…”

Section: Epigenetic Reprograming In Me/cfsmentioning

confidence: 99%

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Epigenetic reprograming in myalgic encephalomyelitis/chronic fatigue syndrome: A narrative of latent viruses

Apostolou,

Rosén

2024

J Intern Med

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic disease presenting with severe fatigue, post‐exertional malaise, and cognitive disturbances—among a spectrum of symptoms—that collectively render the patient housebound or bedbound. Epigenetic studies in ME/CFS collectively confirm alterations and/or malfunctions in cellular and organismal physiology associated with immune responses, cellular metabolism, cell death and proliferation, and neuronal and endothelial cell function. The sudden onset of ME/CFS follows a major stress factor that, in approximately 70% of cases, involves viral infection, and ME/CFS symptoms overlap with those of long COVID. Viruses primarily linked to ME/CFS pathology are the symbiotic herpesviruses, which follow a bivalent latent–lytic lifecycle. The complex interaction between viruses and hosts involves strategies from both sides: immune evasion and persistence by the viruses, and immune activation and viral clearance by the host. This dynamic interaction is imperative for herpesviruses that facilitate their persistence through epigenetic regulation of their own and the host genome. In the current article, we provide an overview of the epigenetic signatures demonstrated in ME/CFS and focus on the potential strategies that latent viruses—particularly Epstein–Barr virus—may employ in long‐term epigenetic reprograming in ME/CFS. Epigenetic studies could aid in elucidating relevant biological pathways impacted in ME/CFS and reflect the physiological variations among the patients that stem from environmental triggers, including exogenous viruses and/or altered viral activity.

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Section: Epigenetic Reprograming In Me/cfsmentioning

confidence: 99%

“…A systematic review by Tziastoudi et al. [72] on gene alterations—common in ME/CFS and long COVID—highlighted the involvement of genes related to inflammation (mediated by chemokine‐ and cytokine‐signaling pathways), T‐cell activation, and Toll‐like receptor–signaling pathways.…”

Section: Epigenetic Reprograming In Me/cfsmentioning

confidence: 99%

Epigenetic reprograming in myalgic encephalomyelitis/chronic fatigue syndrome: A narrative of latent viruses

Apostolou,

Rosén

2024

J Intern Med

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“…It is speculated that the post-viral pathogenesis of PASC may be similar to, or even identical to, that of ME/CFS [1]. A number of researchers have proposed pathophysiological mechanisms that may account for the similarities between ME/CFS and PASC [1][2][3][4][5][6]. The aims of this article are: (i) to indicate the converging evidence that ME/CFS and PASC involve a highly similar constellation of symptoms; (ii) to propose the hypothesis that ME/CFS and PASC have a similar etiology founded on a breakdown of the body's central systems of homeostasis; and (iii) to indicate the possibility that neuroinflammation may be responsible for the dyshomeostasis that occurs in ME/CFS and PASC.…”

Section: Introductionmentioning

confidence: 99%

Converging Evidence of Similar Symptomatology of ME/CFS and PASC Indicating Multisystemic Dyshomeostasis

Marks¹

2023

Biomedicines

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The purpose of this article is to review the evidence of similar symptomatology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and post-acute sequelae of SARS-CoV-2 infection (PASC). Reanalysis of data from a study by Jason comparing symptom reports from two groups of ME/CFS and PASC patients shows a notably similar symptomatology. Symptom scores of the PASC group and the ME/CFS group correlated 0.902 (p < 0.0001) across items. The hypothesis is presented that ME/CFS and PASC are caused by a chronic state of multisystemic disequilibrium including endocrinological, immunological, and/or metabolic changes. The hypothesis holds that a changed set point persistently pushes the organism towards a pathological dysfunctional state which fails to reset. To use an analogy of a thermostat, if the ‘off switch’ of a thermostat intermittently stops working, for periods the house would become warmer and warmer without limit. The hypothesis draws on recent investigations of the Central Homeostasis Network showing multiple interconnections between the autonomic system, central nervous system, and brain stem. The hypothesis helps to explain the shared symptomatology of ME/CFS and PASC and the unpredictable, intermittent, and fluctuating pattern of symptoms of ME/CFS and PASC. The current theoretical approach remains speculative and requires in-depth investigation before any definite conclusions can be drawn.

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Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches

Molnar,

Lehoczki,

Fekete

et al. 2024

GeroScience

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The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has introduced the medical community to the phenomenon of long COVID, a condition characterized by persistent symptoms following the resolution of the acute phase of infection. Among the myriad of symptoms reported by long COVID sufferers, chronic fatigue, cognitive disturbances, and exercise intolerance are predominant, suggesting systemic alterations beyond the initial viral pathology. Emerging evidence has pointed to mitochondrial dysfunction as a potential underpinning mechanism contributing to the persistence and diversity of long COVID symptoms. This review aims to synthesize current findings related to mitochondrial dysfunction in long COVID, exploring its implications for cellular energy deficits, oxidative stress, immune dysregulation, metabolic disturbances, and endothelial dysfunction. Through a comprehensive analysis of the literature, we highlight the significance of mitochondrial health in the pathophysiology of long COVID, drawing parallels with similar clinical syndromes linked to post-infectious states in other diseases where mitochondrial impairment has been implicated. We discuss potential therapeutic strategies targeting mitochondrial function, including pharmacological interventions, lifestyle modifications, exercise, and dietary approaches, and emphasize the need for further research and collaborative efforts to advance our understanding and management of long COVID. This review underscores the critical role of mitochondrial dysfunction in long COVID and calls for a multidisciplinary approach to address the gaps in our knowledge and treatment options for those affected by this condition.

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Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Cited by 4 publications

References 288 publications

Epigenetic reprograming in myalgic encephalomyelitis/chronic fatigue syndrome: A narrative of latent viruses

Epigenetic reprograming in myalgic encephalomyelitis/chronic fatigue syndrome: A narrative of latent viruses

Converging Evidence of Similar Symptomatology of ME/CFS and PASC Indicating Multisystemic Dyshomeostasis

Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches

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