Research reveals genetic links between chronic fatigue syndrome and long COVID
A major new genetic study suggests that myalgic encephalomyelitis, also known as ME or chronic fatigue syndrome, is driven by thousands of small genetic factors working together rather than a single cause. The findings also show a significant overlap with long COVID, strengthening the case that both conditions are rooted in biology rather than misdiagnosis or psychology, Qazinform News Agency correspondent reports, citing medRxiv.
Researchers analyzed genetic data from the DecodeME project, one of the largest studies of ME to date, and compared it with data from healthy volunteers in the UK Biobank. Instead of looking for single genes, the team searched for recurring combinations of genetic changes that appear more often in people with ME.
They identified more than 22,000 such genetic patterns linked to a higher likelihood of having the disease. People with the highest number of these patterns were about one and a half times more likely to have ME than those with the fewest. According to the authors, this shows that ME risk builds up gradually through many small genetic effects rather than one defining marker.
The study linked these genetic patterns to more than 2,300 genes. From these, researchers highlighted 259 key genes that appear most strongly connected to ME. Many of them are involved in immune system responses, brain and nerve communication, cellular stress responses, and signal transmission throughout the body.
Importantly, the researchers also found a strong genetic connection between ME and long COVID. Out of 180 genes previously linked to long COVID in other large studies, 76 were also associated with ME in this analysis. This overlap was far greater than would be expected by chance, suggesting the two conditions share common biological pathways.
The authors stress that ME and long COVID are not the same illness. However, they appear to overlap in some patients, particularly those whose symptoms began after an infection. This may help explain why many people developed ME-like symptoms following COVID infections.
The findings could have practical consequences. By identifying groups of patients who share specific genetic patterns, researchers believe it may become possible to test existing medicines already used for other conditions to see whether they help certain ME patients. This approach could be faster than developing new drugs from scratch.
The study also underlines why a single treatment is unlikely to work for everyone with ME. Since different patients show distinct biological patterns, future care may need to be more personalized.
The research was published as a preprint and has not yet been peer reviewed, meaning the results still require independent confirmation. Even so, patient groups say the study marks an important step toward wider recognition of ME as a serious physical illness and toward more targeted research and treatment in the future.
Earlier, Qazinform News Agency reported that COVID-19 vaccines can trigger heart inflammation.