Mechanistic insights, shared biology, and new routes to diagnosis and treatment
At the International Association of CFS/ME Research and Clinical Conference, Sayoni Das, SVP Bioinformatics at PrecisionLife, presented genetic risk factors and biological commonalities between ME/CFS and Long COVID – two of the most complex and costly chronic conditions affecting millions worldwide.
Watch the highlights
Sayoni Das shares the key results and implications for patients, researchers and healthcare.
Implications for Healthcare and Diagnostics
Identifying shared genetic risk factors between ME/CFS and Long COVID strengthens biological understanding of post-viral fatigue syndromes and highlights opportunities for earlier diagnosis, mechanism-guided therapy, and preventive interventions in millions of patients worldwide.
Findings include:
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First reproducible genetic associations
Using PrecisionLife’s combinatorial analytics, 14 novel genes were identified for ME/CFS (UK Biobank) and 73 for Long COVID (Sano GOLD). -
Shared genetic signatures
Nine genes – including CLOCK and INSR – were found in both conditions, indicating overlapping biological mechanisms such as metabolic stress, insulin signalling, mitochondrial dysfunction, and immune regulation. These shared pathways may explain why some Long COVID patients develop chronic post-viral fatigue syndromes similar to ME/CFS. -
Patient stratification by mechanism
Distinct genetic subgroups correlate with clinical symptoms – for example, AKAP1 variants linked to fatigue and post-exertional malaise, SLC6A11 to cognitive effects, and CLOCK to sleep dysregulation – enabling precision diagnostics and tailored treatment selection. -
Pathways to diagnostics and treatment
The reproducibility of these results across DecodeME and All of Us cohorts supports development of rapid, low-cost genotyping tests to assess disease risk and mechanism, and identifies repurposing candidates targeting insulin and inflammatory pathways.
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