A new study, published in the journal "Translational Medicine," has revealed a common biological mechanism that may explain the chronic fatigue experienced by people with five different diseases.
The study was conducted by researchers from the University of East Anglia and Oxford Biodynamics, in collaboration with the London School of Hygiene and Tropical Medicine and the Cornwall Partnership of the British National Health Service.
The diseases involved include: long COVID, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), post-traumatic stress disorder, rheumatoid arthritis, and multiple sclerosis.
Despite the different causes of these diseases, those affected may experience similar symptoms, most notably extreme fatigue, mental confusion, poor concentration, sleep disturbances, and a reduced ability to perform daily activities. The researchers wanted to determine whether this similarity in symptoms was linked to shared biological mechanisms.
To answer this, the team used Oxford Biodynamics’ EpiSwitch Orion platform, which allows for the study of the genome’s three-dimensional structure, rather than simply analyzing the DNA sequence.
The researchers used genomic data from previous studies involving the five cases and examined how genes interact within cells. The results showed that direct overlap between disease-associated genes was limited, but when analyzed within biological networks, clear common links emerged.
These links were concentrated in systems responsible for regulating immunity and inflammation, energy production within mitochondria, metabolism, stress response, and neuroendocrine signaling.
Professor Dmitry Pshetzitzky, the lead researcher in the study, said that these results suggest that diseases with different causes may ultimately affect the same biological systems, which may explain the similarity of symptoms between them.
The researchers also identified several key genes in these networks, including LAG3, which is associated with the exhaustion of T cells after prolonged activation. However, they emphasized that the role of these genes requires further investigation to confirm.
Researchers believe that disruptions to these networks may help explain the persistence of fatigue in some patients even after the initial trigger for the illness has subsided. In long COVID, for example, some immune responses may persist after infection, while psychological trauma can affect stress hormone pathways and inflammatory responses. Although these triggers differ, their effects may overlap in pathways responsible for energy production and immune regulation.
The findings could pave the way for the development of blood tests that can help diagnose these conditions more objectively. Currently, the diagnosis of myalgic encephalomyelitis/chronic fatigue syndrome and long COVID relies heavily on symptoms, as there is no universally accepted laboratory test for their diagnosis.
A previous study using the EpiSwitch platform showed promising results for a blood test for chronic fatigue syndrome/myalgic encephalomyelitis, but it still needs further verification before it can be used clinically.
Pshetzky said the researchers hope the new findings will help develop biomarkers that can be used for diagnosis, and in the longer term lead to treatments that target the biological pathways common to these conditions.
The researchers stressed that the results do not mean that the five diseases are one disease, but rather indicate the possibility that they share biological mechanisms that may explain some of the similar symptoms, most notably chronic fatigue.
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