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Genetic biomarkers shared by ME/CFS and COVID-19

In September, ME Research UK attended the ME Genetics Research Symposium held at the Human Genetics Unit in the University of Edinburgh, and provided readers with an overview of the DeCode MEproject and the latest developments in the field.

Following that, a recently published study in Annals of Clinical and Translational Neurology explores the possible genetic overlap between ME/CFS and COVID-19.

The two conditions present with some similar symptoms, such as physical and mental fatigue, but also some differences, such as shortness of breath being a feature of COVID-19 and long COVID. A team of researchers in Greece and the USA set out to ascertain whether or not the two illnesses share any underlying common genetic markers.

Systematic review

The researchers carried out a systematic review of published research to extract relevant data from genetic association studies, either in candidate genes or in genome-wide and cohort studies. They then performed a variety of different analyses (gene ontology and pathway analysis) to identify genetic markers that were common to both ME/CFS and COVID-19.

The review included 26 studies in people with ME/CFS and 71 studies in people with COVID-19, and significant results were found for 429 genes in ME/CFS and for 97 genes in COVID-19.

A number of genes were found to be common to both conditions, and these included ACEHLA-AHLA-C,HLA-DQA1HLA-DRB1 and TYK2. In general, the overlapping genes appear to be related to immune processes, including inflammation mediated by chemokine and cytokine signalling pathways, and T-cell activation and Toll receptor signalling pathways.

These terms may be familiar to ME/CFS sufferers as we often read about a ‘cytokine storm’ in ME/CFS, or the role of immune cells like T cells.

Overall, the results suggest that the way in which both ME/CFS and long COVID develop involves a degree of immune dysfunction related to those identified overlapping genes.

Possible treatments?

Given the potential involvement of immune activation genes, the researchers conclude by suggesting some pharmacological agents that might be considered in the management of ME/CFS and/or long COVID. For example, natural flavonoids regulate the immune response, while luteolin inhibits both microglia and the unique tissue immune cells, or mast cells. Luteolin may help reduce neuroinflammation and cognitive dysfunction or brain-fog. However, this is mainly speculative, and all potential treatments would need to be rigorously tested in randomised controlled trials.

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