Evidence map›Paper›PMID 30564562›Full record

ReviewFrontiers in pediatrics2018

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome in the Era of the Human Microbiome: Persistent Pathogens Drive Chronic Symptoms by Interfering With Host Metabolism, Gene Expression, and Immunity.

Amy Proal, Trevor Marshall

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pediatrics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 5 pooled it
7.2field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 5 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Systematic review with meta-analysis of active herpesvirus infections in patients with COVID-19: Old players on the new field.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2023
    Pooled it
  2. Pooled it
  3. Fatigue Symptoms Associated With COVID-19 in Convalescent or Recovered COVID-19 Patients; a Systematic Review and Meta-Analysis.Annals of behavioral medicine : a publication of the Society of Behavioral Medicine · 2022
    Pooled it
  4. Pooled it
  5. Pooled it
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  13. Targeting the SARS-CoV-2 reservoir in long COVID.The Lancet. Infectious diseases · 2025
    Review
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  18. Systems-level temporal immune-metabolic profile in Crimean-Congo hemorrhagic fever virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

2 authors at 1 institution in 1 country.

Amy ProalAutoimmunity Research Foundation, Thousand Oaks, CA, United States.
Trevor MarshallAutoimmunity Research Foundation, Thousand Oaks, CA, United States.
Autoimmunity Research Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The illness ME/CFS has been repeatedly tied to infectious agents such as Epstein Barr Virus. Expanding research on the human microbiome now allows ME/CFS-associated pathogens to be studied as interacting members of human microbiome communities. Humans harbor these vast ecosystems of bacteria, viruses and fungi in nearly all tissue and blood. Most well-studied inflammatory conditions are tied to dysbiosis or imbalance of the human microbiome. While gut microbiome dysbiosis has been identified in ME/CFS, microbes and viruses outside the gut can also contribute to the illness. Pathobionts, and their associated proteins/metabolites, often control human metabolism and gene expression in a manner that pushes the body toward a state of illness. Intracellular pathogens, including many associated with ME/CFS, drive microbiome dysbiosis by directly interfering with human transcription, translation, and DNA repair processes. Molecular mimicry between host and pathogen proteins/metabolites further complicates this interference. Other human pathogens disable mitochondria or dysregulate host nervous system signaling. Antibodies and/or clonal T cells identified in patients with ME/CFS are likely activated in response to these persistent microbiome pathogens. Different human pathogens have evolved similar survival mechanisms to disable the host immune response and host metabolic pathways. The metabolic dysfunction driven by these organisms can result in similar clusters of inflammatory symptoms. ME/CFS may be driven by this pathogen-induced dysfunction, with the nature of dysbiosis and symptom presentation varying based on a patient's unique infectious and environmental history. Under such conditions, patients would benefit from treatments that support the human immune system in an effort to reverse the infectious disease process.

Indexed as

autoantibodydysbiosisgut-brain axisholobiontME/CFSmicrobiomemolecular mimicrypathobiont

Identifiers

PMID30564562
PMCPMC6288442
OpenAlexW2903546985

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.