Evidence map›Paper›PMID 36982194›Full record

ReviewInternational journal of molecular sciences2023

Towards a Better Understanding of the Complexities of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Long COVID.

Warren P Tate, Max O M Walker, Katie Peppercorn, Anna L H Blair, Christina D Edgar

Open access · goldFull text readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
8.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Urinary metabolites and fatigue in a population-based metabolomics study: an exploratory analysis.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Observational
  10. Article
  11. Review
  12. Application of DNA Methylome Analysis to Patients with ME/CFS.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Warren P TateDepartment of Biochemistry, School of Biomedical Sciences, Division of Health Sciences, University of Otago, Dunedin 9054, New Zealand.ORCID 0000-0002-6971-7734
Max O M WalkerDepartment of Biochemistry, School of Biomedical Sciences, Division of Health Sciences, University of Otago, Dunedin 9054, New Zealand.ORCID 0009-0002-0173-5482
Katie PeppercornDepartment of Biochemistry, School of Biomedical Sciences, Division of Health Sciences, University of Otago, Dunedin 9054, New Zealand.
Anna L H BlairDepartment of Biochemistry, School of Biomedical Sciences, Division of Health Sciences, University of Otago, Dunedin 9054, New Zealand.
Christina D EdgarDepartment of Biochemistry, School of Biomedical Sciences, Division of Health Sciences, University of Otago, Dunedin 9054, New Zealand.
University of Otago · NZ

Funding

ANZMES -NZA ME/CFS natiuonal disease advisory association no grant number
6 · The paper itself

Abstract

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex condition arising in susceptible people, predominantly following viral infection, but also other stressful events. The susceptibility factors discussed here are both genetic and environmental although not well understood. While the dysfunctional physiology in ME/CFS is becoming clearer, understanding has been hampered by different combinations of symptoms in each affected person. A common core set of mainly neurological symptoms forms the modern clinical case definition, in the absence of an accessible molecular diagnostic test. This landscape has prompted interest in whether ME/CFS patients can be classified into a particular phenotype/subtype that might assist better management of their illness and suggest preferred therapeutic options. Currently, the same promising drugs, nutraceuticals, or behavioral therapies available can be beneficial, have no effect, or be detrimental to each individual patient. We have shown that individuals with the same disease profile exhibit unique molecular changes and physiological responses to stress, exercise and even vaccination. Key features of ME/CFS discussed here are the possible mechanisms determining the shift of an immune/inflammatory response from transient to chronic in ME/CFS, and how the brain and CNS manifests the neurological symptoms, likely with activation of its specific immune system and resulting neuroinflammation. The many cases of the post viral ME/CFS-like condition, Long COVID, following SARS-CoV-2 infection, and the intense research interest and investment in understanding this condition, provide exciting opportunities for the development of new therapeutics that will benefit ME/CFS patients.

Indexed as

COVID-19Fatigue Syndrome, ChronicCausalityHumansPost-Acute COVID-19 SyndromeSARS-CoV-2disease modelsdisease subtype/phenotypeLong COVIDME/CFSneuroinflammationsusceptibilitysystemic inflammationtherapeutics

Identifiers

PMID36982194
PMCPMC10048882
OpenAlexW4323566375

What OpenQuestion holds

Textfull text, public
LicenceCC BY
reference markers read1
measurements read21
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.