IMAGE DESCRIPTION: A image of Covid spike proteins with two circles, one with a person with ME/CFS and the other an image of DNA. The title: Genetic risk factors for Long Covid and ME/CFS - research findings from Precision Life with the PrecisionLife logo (bottom left). The ME Association logo (bottom right).

Genetic risk factors for Long Covid and ME/CFS – research findings from Precision Life

PrecisionLife has shared an article on their website ‘PrecisionLife Identifies First Detailed Genetic Risk Factors' which highlights genes from their Long Covid research that have been compared to ME/CFS.


The analysis identified 73 genes that were highly associated with severe and fatigue dominant forms of the disease. Of these, 9 genes have prior associations to acute COVID-19 and 14 were differentially expressed in a transcriptomic analysis of Long Covid patients.

To understand similarities with other post-viral, fatigue and other complex disorders, PrecisionLife compared the results of its long COVID analysis against known genetic associations across a range of over 170 neurological, cardiovascular, gastrointestinal, autoimmune, and metabolic diseases.

This cross-disease analysis highlighted Long Covid risk genes that were also implicated in a wide range of diseases and found that 9 genes associated with Long Covid were also found in a recent combinatorial analysis of ME/CFS patients.

The ME Association's statement

We know that there are a number of important symptoms and pathological overlaps between Long Covid and ME/CFS. These are also common to many other post-viral diseases where previously healthy people fail to recover from a viral infection.

We also know that there may well be a genetic predisposition to developing Long Covid and ME/CFS. This genetic link is currently being investigated in the DecodeME study – where Professor Chris Ponting and his genetics team at the University of Edinburgh are analysing genetic material (DNA) from over 20,000 people with ME/CFS.

Whilst the findings from Precision Health are interesting and point towards a genetic component they need to be replicated in much larger studies, including DecodeME, before any firm conclusions can be drawn as to which genes may be involved and which body systems they may be affecting.

When we have this information it may then provide some useful information regarding both the repositioning of current drugs to treat both Long Covid and ME/CFS and the development of new drug treatments for post-viral disease.

Further reading:

Dr Charles Shepherd,
Trustee and
Hon. Medical Adviser
to the ME Association.

Dr Charles Shepherd
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