On August 22nd, 2026, a new paper was published in the Journal of Translational Medicine, “Beyond genes: EpiSwitch® and Orion platform-powered 3D genome architecture biomarkers reveal shared biology across ME/CFS, long COVID, PTSD, rheumatoid arthritis, and multiple sclerosis.”
AI Summary:
- What they did: Researchers compared ME/CFS, Long COVID, PTSD, rheumatoid arthritis and multiple sclerosis using existing genetic data alongside 3D genomics, which looks at how different regions of DNA interact and potentially influence gene activity. They mapped these DNA interaction sites to genes and used computational tools to analyse how the genes and proteins were connected into larger biological networks.
- What they found: Although the conditions shared relatively few individual genes, the researchers found some overlap in broader biological pathways, particularly immune/cytokine signalling, interferon responses, mitochondrial function and metabolism. They also highlighted genes such as LAG3 and parts of the mTOR pathway as highly connected within these networks.
- What it means: The researchers suggest that these illnesses may involve disturbances in interconnected biological systems, rather than having completely separate mechanisms. However, this was largely a computational, association-based analysis, so it doesn't demonstrate that these pathways cause the illnesses or establish that the proposed biomarkers or treatment targets will work in patients.
ME Association Comment:
This is an interesting and quite complex research hypothesis.
It links our current understanding of the genetics of several diseases – ME/CFS, Long Covid, multiple sclerosis, rheumatoid arthritis – that involve debilitating fatigue, cognitive dysfunction and other symptoms, and which appear to be related to abnormalities involving the brain, immune system function and energy production in cellular structures called mitochondria.
As Professor Dmitry Pshezhetskiy points out, research like this which is aimed at increasing our understanding of underlying disease mechanisms through the analysis of cellular genetic material called DNA, could lead to both diagnostic biomarkers and treatments that are aimed at disease causation and not just symptoms.
However, I would have preferred the researchers to make it clearer that while more research is required the conclusions they are making here are still quite speculative and unproven at this point in time.
Professor Chris Ponting has provided some expert comment on the genetics to the Science Media Centre:
The UK ME/CFS Biobank, which is funded by the MEA Ramsay Research Fund, has supplied blood samples for some of Professor Dmitry Pshezhetskiy's research.
Dr Charles Shepherd,
Trustee and Hon. Medical Adviser to the ME Association,
Member of the 2018-2021 NICE guideline on ME/CFS committee,
Member of the 2002 Chief Medical Officer's Working Group on ME/CFS
