Genome-epigenome interactions associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Herrera, Santiago; Vega, Wilfred C. de; Ashbrook, David G.; Vernon, Suzanne D.; McGowan, Patrick O.

doi:10.1080/15592294.2018.1549769

Cited by 31 publications

(69 citation statements)

References 77 publications

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“…In line with this theory, it should be noted that during the preparation of the current manuscript, McGowan's group published the results of a methylation genome-wide study including a screening of~4.3 million single nucleotide polymorphisms in 61 patients with ME/CFS and 48 matched healthy control subjects; they found significant genome-epigenome interactions associated with, and possibly involved in, the mechanisms of this disease. 71 This finding further supports the idea that genome-wide methylation studies must be analyzed in the context of genomic individual polymorphisms.…”

Section: April 2019supporting

confidence: 66%

“…Although a paucity of studies aiming at evaluation of the ME/CFS epigenome was found, a total of 230 CFS and 115 healthy control subject samples have already been assayed by genome-wide DNA methylation approaches, upon including the recent study by the McGowan's group 71 ; and a total of 127 CFS and 128 healthy control subjects have been tested for ncRNA DE by multiplex assays. Heterogeneity of studies, however, limits study value for stratified TE screenings, calling for further efforts.…”

Section: Discussionmentioning

confidence: 99%

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Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Almenar-Pérez

Ovejero

Sánchez-Fito

et al. 2019

Clinical Therapeutics

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Purpose: Studies to determine epigenetic changes associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) remain scarce; however, current evidence clearly shows that methylation patterns of genomic DNA and noncoding RNA profiles of immune cells differ between patients and healthy subjects, suggesting an active role of these epigenetic mechanisms in the disease. The present study compares and contrasts the available ME/CFS epigenetic data in an effort to evidence overlapping pathways capable of explaining at least some of the dysfunctional immune parameters linked to this disease. Methods: A systematic search of the literature evaluating the ME/CFS epigenome landscape was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. Differential DNA methylation and noncoding RNA differential expression patterns associated with ME/CFS were used to screen for the presence of transposable elements using the Dfam browser, a search program nurtured with the Repbase repetitive sequence database and the RepeatMasker annotation tool. Findings: Unexpectedly, particular associations of transposable elements and ME/CFS epigenetic hallmarks were uncovered. A model for the disease emerged involving transcriptional induction of endogenous dormant transposons and structured cellular RNA interactions, triggering the activation of the innate immune system without a concomitant active infection. Implications: Repetitive sequence filters (ie, RepeatMasker) should be avoided when analyzing transcriptomic data to assess the potential participation of repetitive sequences ("junk repetitive DNA"), representing >45% of the human genome, in the onset and evolution of ME/CFS. In addition, transposable element screenings aimed at designing cost-effective, focused empirical assays that can confirm or disprove the suspected involvement of transposon transcriptional activation in this disease, following the pilot strategy presented here, will require databases gathering large ME/CFS epigenetic datasets.

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Section: April 2019supporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Almenar-Pérez

Ovejero

Sánchez-Fito

et al. 2019

Clinical Therapeutics

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“…The addition of methyl groups at promoters may contribute to a hypometabolic state by down-regulating the expression of genes involved in key metabolic pathways. The ME/CFS phenotype is linked to differential methylation in genes associated with immune function and cellular metabolism [48,65,66]. For example, a 2017 study [48] detected 12,608 differentially methylated sites predominantly at cellular metabolism genes, changes that also could be related to patient quality of life health scores.…”

Section: Global Research Into Me/cfs Biologymentioning

confidence: 99%

Current Research Provides Insight into the Biological Basis and Diagnostic Potential for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

et al. 2019

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe fatigue illness that occurs most commonly following a viral infection, but other physiological triggers are also implicated. It has a profound long-term impact on the life of the affected person. ME/CFS is diagnosed primarily by the exclusion of other fatigue illnesses, but the availability of multiple case definitions for ME/CFS has complicated diagnosis for clinicians. There has been ongoing controversy over the nature of ME/CFS, but a recent detailed report from the Institute of Medicine (Academy of Sciences, USA) concluded that ME/CFS is a medical, not psychiatric illness. Importantly, aspects of the biological basis of the ongoing disease have been revealed over the last 2–3 years that promise new leads towards an effective clinical diagnostic test that may have a general application. Our detailed molecular studies with a preclinical study of ME/CFS patients, along with the complementary research of others, have reported an elevation of inflammatory and immune processes, ongoing neuro-inflammation, and decreases in general metabolism and mitochondrial function for energy production in ME/CFS, which contribute to the ongoing remitting/relapsing etiology of the illness. These biological changes have generated potential molecular biomarkers for use in diagnostic ME/CFS testing.

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“…169 Specific DNA methylation patterns have been detected in response to the external and internal environment (e.g., stress). [170][171][172] DNA methylation patterns change with age, smoking, and disease states, including in hypoxic conditions. [173][174][175] The silent hypoxemia observed with some COVID-19 patients may lead to alterations in DNA methylation patterns.…”

Section: Epigenetic Basicsmentioning

confidence: 99%

“…Specific DNA methylation patterns have been detected in response to the external and internal environment (e.g., stress). [170][171][172] In response to trauma and chronic stress, there are epigenetic changes in DNA methylation that alter gene expression and modulate the stress response. Post-traumatic stress disorder (PTSD) is a mental disorder that develops after a person is exposed to a traumatic event such as sexual assault, bank robbery, warfare, and abuse.…”

Section: Stress and Epigeneticsmentioning

confidence: 99%

SARS‐CoV‐2 multifaceted interaction with the human host. Part II: Innate immunity response, immunopathology, and epigenetics

Beacon

Su²,

Lakowski

et al. 2020

IUBMB Life

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The SARS-CoV-2 makes its way into the cell via the ACE2 receptor and the proteolytic action of TMPRSS2. In response to the SARS-CoV-2 infection, the innate immune response is the first line of defense, triggering multiple signaling pathways to produce interferons, pro-inflammatory cytokines and chemokines, and initiating the adaptive immune response against the virus. Unsurprisingly, the virus has developed strategies to evade detection, which can result in delayed, excessive activation of the innate immune system. The response elicited by the host depends on multiple factors, including health status, age, and sex. An overactive innate immune response can lead to a cytokine storm, inflammation, and vascular disruption, leading to the vast array of symptoms exhibited by COVID-19 patients. What is known about the expression and epigenetic regulation of the ACE2 gene and the various players in the host response are explored in this review.

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Genome-epigenome interactions associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Cited by 31 publications

References 77 publications

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Current Research Provides Insight into the Biological Basis and Diagnostic Potential for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

SARS‐CoV‐2 multifaceted interaction with the human host. Part II: Innate immunity response, immunopathology, and epigenetics

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