Plate Nº 11 · recorded October 10, 2026
Health & Medicine ResearchReported finding
Five chronic illnesses may share a common biological root, study finds
Published October 1, 2026, a study suggests ME/CFS, long Covid, PTSD, rheumatoid arthritis, and multiple sclerosis disrupt shared biological networks governing immunity, energy, and metabolism.
By James Calloway3 min read657 words
In brief
- Published October 1, 2026 in the Journal of Translational Medicine (DOI: 10.1186/s12967-026-08874-9)
- Analyzed five conditions: ME/CFS, long Covid, PTSD, rheumatoid arthritis, and multiple sclerosis
- Used Oxford BioDynamics' EpiSwitch® Orion platform to map 3D genome contact points
- Highlighted LAG3 as a candidate gene linked to ME/CFS and T-cell exhaustion
- Led by the University of East Anglia with Oxford BioDynamics, London School of Hygiene and Tropical Medicine, and Cornwall Partnership NHS Foundation Trust
A study published on October 1, 2026 identifies shared biological networks across five conditions long treated as separate illnesses: ME/CFS, long Covid, PTSD, rheumatoid arthritis, and multiple sclerosis. Researchers analyzed three-dimensional genome architecture rather than linear DNA sequences to reveal the overlap.
The work, led by the University of East Anglia with Oxford BioDynamics, the London School of Hygiene and Tropical Medicine, and Cornwall Partnership NHS Foundation Trust, appears in the Journal of Translational Medicine.
What did the researchers find?
The team combined previously published genomic data from genome-wide association studies for long Covid, PTSD, rheumatoid arthritis, and multiple sclerosis with 3D genomic data from an earlier ME/CFS study. They applied Oxford BioDynamics' EpiSwitch® Orion platform throughout.
"DNA is folded in our cells, so regions far apart in the linear sequence can touch, and those contact points are where genes get controlled," said Dr Ewan Hunter, Chief Data Officer at Oxford BioDynamics.
At the individual gene level, the conditions showed little direct overlap. A different picture emerged when the team analyzed how those genes interact within biological networks.
"We expected to find at least some overlap in genes across the conditions. But we actually found the opposite," said lead researcher Prof Dmitry Pshezhetskiy of UEA's Norwich Medical School.
"But when we analyzed how those genes interact in complex biological networks, a completely different picture emerged. Suddenly, the diseases appeared deeply connected."
Why do these conditions share symptoms?
The five illnesses begin in very different ways: viral infection (ME/CFS and long Covid), psychological trauma (PTSD), and autoimmune activity (rheumatoid arthritis and MS). Yet patients report strikingly similar complaints.
Common reported symptoms include:
- Overwhelming fatigue
- Brain fog and poor concentration
- Disturbed sleep
- Autonomic dysfunction
- A dramatic reduction in everyday functioning
"What we discovered is something approaching a biological unifying theory of fatigue," Pshezhetskiy said.
The team proposes that different triggers converge on common biological circuits controlling energy production, immune regulation, and cellular resilience. A Covid infection can trigger prolonged immune activation. Traumatic stress can disrupt stress-hormone and inflammatory pathways. Both disturbances appear capable of hitting the same downstream systems.
Which biological systems appear most disrupted?
The shared networks center on several major systems:
- Immune and inflammatory signaling
- Mitochondrial energy production
- Metabolic regulation
- Stress-response mechanisms
- Neuroendocrine signaling
The researchers also identified "hub genes" sitting at especially active points within these networks. One gene, LAG3, stood out for ME/CFS. Scientists have previously linked LAG3 to T-cell exhaustion, a state in which immune cells become less effective after remaining activated for an extended period.
The team describes LAG3's role as a candidate finding. Confirming its actual function in chronic fatigue will require further laboratory and clinical work.
Could this lead to blood tests and new treatments?
Doctors today diagnose ME/CFS and long Covid largely through patient-reported symptoms. No universally accepted laboratory test exists, leaving many patients waiting years for answers.
Earlier work using the EpiSwitch platform produced a blood-based ME/CFS test with promising diagnostic accuracy. That test still awaits further validation before clinical use.
"We hope our work could pave the way for objective blood tests capable of identifying underlying biological signatures rather than relying solely on patient-reported symptoms," Pshezhetskiy said.
The researchers also see implications for treatment. If different disorders disturb common networks, drugs targeting those networks might help patients across several conditions, not just one.
What are the limits of the work?
The analysis was computational, not based on newly collected patient samples. The team combined previously published datasets rather than recruiting a new cohort. Candidate hub genes still need functional confirmation in cells and animals.
The authors explicitly frame their findings as a framework for further investigation rather than a finished explanation. Diagnostic blood tests and network-targeted treatments remain future possibilities rather than current tools.
Hunter et al., Journal of Translational Medicine, 2026; 24(1), DOI: 10.1186/s12967-026-08874-9.
via dx.doi.org (Original)
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