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Biomolecules
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Biomarkers in Chronic Fatigue Syndrome (ME/CFS)
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Biomarkers in Chronic Fatigue Syndrome (ME/CFS)

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 23184

Special Issue Editor

Dr. Bhupesh K. Prusty

E-Mail Website
Guest Editor
Julius-Maximilians-Universität Würzburg, Wurzburg, Germany
Interests: herpesviruses; small RNAs; mitochondrial dysfunction; host-pathogen interaction; microbial pathogenesis

Special Issue Information

Dear Colleagues,

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a systemic disease that affects the central nervous system, the immune system, cell energy metabolism, the autonomic nervous system, etc. The main clinical sign is persistent chronic fatigue that is not relieved by rest and lasts for more than six months. Up to 75% of patients are completely unable to work and remain wheelchair-dependent, and at least 25% are permanently housebound or even bedbound. Accordingly, the socio-economic impact of the disease is huge. At present, no curative treatment options are available. Therefore, patients have practically no prospect of recovery or at least of returning to work. Etiological factors for ME/CFS include genetic predisposition, stress, trauma, exposure to toxins, the ratio of physical activity to rest, and a recent history of infectious disease. ME/CFS can affect individuals from all races, genders, age groups, and social statuses. The pathogenesis of ME/CFS is likely multi-factorial and various microbial and viral infections can serve as possible triggers for ME/CFS. However, to date, no single biomarker has been identified that can be generalized to the entire patient population. Considering the heterogeneity of ME/CFS, it is plausible that a specific set of biomarkers might enable us to define disease subtypes. Identification of biomarkers will allow for prognosis of the disease’s development and promote the development of a specific definition for diagnostics and a treatment plan. Hence, I encourage researchers from diverse backgrounds (clinics, systems medicine, genetics, molecular biology, epidemiology) to contribute original research and review articles on any aspect of biomarker identification, biomarker characterization, or translational approaches of clinical relevance to this Special Issue, which aims to bring ideas from different fields of science to one common platform that may stimulate further research and solve a modern day clinical mystery.

Dr. Bhupesh K. Prusty
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Herpesviruses
  • Small RNAs
  • Mitochondrial dysfunction
  • Host-pathogen interaction
  • microbial pathogenesis

Published Papers (3 papers)

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Research

11 pages, 1323 KiB  
Article
Evaluation of Immune Dysregulation in an Austrian Patient Cohort Suffering from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
by Lena Lutz, Johanna Rohrhofer, Sonja Zehetmayer, Michael Stingl and Eva Untersmayr
Biomolecules 2021, 11(9), 1359; https://doi.org/10.3390/biom11091359 - 14 Sep 2021
Cited by 7 | Viewed by 7002
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe multi-systemic disease characterized by debilitating fatigue that is not relieved by rest. The causes of the disease are still largely unexplained, and no causative treatment is currently available. Changes in the immune response are considered [...] Read more.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe multi-systemic disease characterized by debilitating fatigue that is not relieved by rest. The causes of the disease are still largely unexplained, and no causative treatment is currently available. Changes in the immune response are considered as fundamental in the development of ME/CFS. Thus, we aimed to evaluate the immunological profile of ME/CFS patients in a retrospective data analysis. As part of the routine workup for ME/CFS patients, a differential blood count, leukocyte subtyping, and quantification of immunoglobulins and IgG subclasses, as well as a complement analysis, was performed. Out of 262 ME/CFS patients, 64.9% had a reduction or deficiency in at least one of the listed immune parameters. In contrast, 26.3% showed signs of immune activation or inflammation. A total of 17.6% of the ME/CFS patients had an unclassified antibody deficiency, with IgG3 and IgG4 subclass deficiencies as the most common phenotypes. Reduced MBL (mannose-binding lectin) levels were found in 32% of ME/CFS patients, and MBL deficiency in 7%. In summary, the present results confirmed the relevance of immune dysfunction in ME/CFS patients underlining the involvement of a dysfunctional immune response in the disease. Thus, immune parameters are relevant disease biomarkers, which might lead to targeted therapeutic approaches in the future. Full article
(This article belongs to the Special Issue Biomarkers in Chronic Fatigue Syndrome (ME/CFS))
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10 pages, 1342 KiB  
Article
Potential of Activin B as a Clinical Biomarker in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
by Sabine Gravelsina, Zaiga Nora-Krukle, Anda Vilmane, Simons Svirskis, Katrine Vecvagare, Angelika Krumina and Modra Murovska
Biomolecules 2021, 11(8), 1189; https://doi.org/10.3390/biom11081189 - 11 Aug 2021
Cited by 7 | Viewed by 2739
Abstract
Reliable serum biomarkers are of immense need for diagnostic purposes of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)—a disabling and complex disease for which diagnosis is mainly based on clinical symptoms. The aim of this study was to evaluate a possible diagnostic potential of activin [...] Read more.
Reliable serum biomarkers are of immense need for diagnostic purposes of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)—a disabling and complex disease for which diagnosis is mainly based on clinical symptoms. The aim of this study was to evaluate a possible diagnostic potential of activin B by directly comparing 134 cases of ME/CFS with 54 healthy controls. Analyses of human activin B level in plasma samples were performed using a validated human activin B ELISA assay. The results of the study show that activin B levels did not differ statistically significantly between ME/CFS patients and healthy controls (p = 0.6511). No gender or age-related differences in activin B levels were observed in the ME/CFS group and healthy controls. The level of activin B tended to decrease with increasing visual analogue scale score (r = −0.2004; p = 0.5085) nevertheless the results obtained so far does not support the clinical utility of activin B as a biomarker for ME/CFS. Full article
(This article belongs to the Special Issue Biomarkers in Chronic Fatigue Syndrome (ME/CFS))
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20 pages, 2976 KiB  
Article
Bioenergetic and Proteomic Profiling of Immune Cells in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients: An Exploratory Study
by Paula Fernandez-Guerra, Ana C. Gonzalez-Ebsen, Susanne E. Boonen, Julie Courraud, Niels Gregersen, Jesper Mehlsen, Johan Palmfeldt, Rikke K. J. Olsen and Louise Schouborg Brinth
Biomolecules 2021, 11(7), 961; https://doi.org/10.3390/biom11070961 - 29 Jun 2021
Cited by 13 | Viewed by 10426
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous, debilitating, and complex disease. Along with disabling fatigue, ME/CFS presents an array of other core symptoms, including autonomic nervous system (ANS) dysfunction, sustained inflammation, altered energy metabolism, and mitochondrial dysfunction. Here, we evaluated patients’ symptomatology [...] Read more.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous, debilitating, and complex disease. Along with disabling fatigue, ME/CFS presents an array of other core symptoms, including autonomic nervous system (ANS) dysfunction, sustained inflammation, altered energy metabolism, and mitochondrial dysfunction. Here, we evaluated patients’ symptomatology and the mitochondrial metabolic parameters in peripheral blood mononuclear cells (PBMCs) and plasma from a clinically well-characterised cohort of six ME/CFS patients compared to age- and gender-matched controls. We performed a comprehensive cellular assessment using bioenergetics (extracellular flux analysis) and protein profiles (quantitative mass spectrometry-based proteomics) together with self-reported symptom measures of fatigue, ANS dysfunction, and overall physical and mental well-being. This ME/CFS cohort presented with severe fatigue, which correlated with the severity of ANS dysfunction and overall physical well-being. PBMCs from ME/CFS patients showed significantly lower mitochondrial coupling efficiency. They exhibited proteome alterations, including altered mitochondrial metabolism, centred on pyruvate dehydrogenase and coenzyme A metabolism, leading to a decreased capacity to provide adequate intracellular ATP levels. Overall, these results indicate that PBMCs from ME/CFS patients have a decreased ability to fulfill their cellular energy demands. Full article
(This article belongs to the Special Issue Biomarkers in Chronic Fatigue Syndrome (ME/CFS))
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