Englebienne, P, Verhas, M, Herst, C V et al. · Medical hypotheses · 2003 · DOI
This study proposes a potential explanation for why some ME/CFS patients experience severe fatigue despite having normal thyroid blood tests. The researchers suggest that certain immune proteins called interferons may trigger the production of other proteins that interfere with thyroid hormone function at the cellular level, making the body behave as if it has low thyroid activity even though standard thyroid tests appear normal.
This work addresses a clinically significant observation that many ME/CFS patients experience hypothyroid-like symptoms without abnormal thyroid hormone levels. If supported by experimental evidence, this mechanism could explain fatigue and metabolic dysfunction in a subset of patients and suggest potential therapeutic targets in the interferon pathway.
This is a theoretical hypothesis without experimental validation—no data directly demonstrate that 2-5OASL proteins actually function as thyroid receptor corepressors or that this mechanism occurs in ME/CFS patients. The study does not establish causation, prove the mechanism occurs in vivo, or demonstrate clinical relevance in an actual patient population. Correlation between interferon dysregulation and fatigue does not prove this specific mechanism is responsible.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
The first block is for the primary paper and is the citation you should use in research work. The atlas-snapshot line only applies if you are specifically referring to this atlas’s reading of the paper on the date shown.
Primary citation
Englebienne, P, Verhas, M, Herst, C V, & De Meirleir, K (2003). Type I interferons induce proteins susceptible to act as thyroid receptor (TR) corepressors and to signal the TR for destruction by the proteasome: possible etiology for unexplained chronic fatigue.. Medical hypotheses. https://doi.org/10.1016/s0306-9877(02)00353-5
BibTeX
@article{mecfsatlas-englebienne-2003-type-interferons,
author = {Englebienne, P and Verhas, M and Herst, C V and De Meirleir, K},
title = {Type I interferons induce proteins susceptible to act as thyroid receptor (TR) corepressors and to signal the TR for destruction by the proteasome: possible etiology for unexplained chronic fatigue.},
journal = {Medical hypotheses},
year = {2003},
doi = {10.1016/s0306-9877(02)00353-5},
note = {PubMed: 12606231},
url = {https://www.mecfsatlas.com/evidence/englebienne-2003-type-interferons},
}Atlas snapshot reference
ME/CFS Atlas. Generator v1 / Scanner v1.4 / policy v0.1. Accessed 2026-05-30. https://www.mecfsatlas.com/evidence/englebienne-2003-type-interferons
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