COVID-19: A methyl-group assault? by Andrew McCaddon, Björn Regland in Medical Hypotheses Vol 149, Apr 2021, 110543 [ doi.org/10.1016/j.mehy.2021.110543]

Research abstract:

The socio-economic implications of COVID-19 are devastating. Considerable morbidity is attributed to ‘long-COVID’ – an increasingly recognized complication of infection. Its diverse symptoms are reminiscent of vitamin B12 deficiency, a condition in which methylation status is compromised.

We suggest why SARS-CoV-2 infection likely leads to increased methyl-group requirements and other disturbances of one-carbon metabolism. We propose these might explain the varied symptoms of long-COVID. Our suggested mechanism might also apply to similar conditions such as myalgic encephalomyelitis/chronic fatigue syndrome.

The hypothesis is evaluable by detailed determination of vitamin B12 and folate status, including serum formate as well as homocysteine and methylmalonic acid, and correlation with viral and host RNA methylation and symptomatology. If confirmed, methyl-group support [supplementation] should prove beneficial in such individuals.

Conclusion

We suggest that SARS-CoV-2 induces an increased demand for methyl-groups whilst simultaneously impairing their supply due to viral-induced oxidative stress.

The biochemical implications of our hypothesis might explain the diverse symptoms experienced by patients with long-COVID and, if confirmed, suggests possible approaches to treatment.

It would be ironic if the socio-economic devastation of COVID-19, by intensifying world-wide research in a viral pandemic, leads to valuable insights into other conditions such as ME/CFS, as well as providing additional clues to the aetiology of memory disorders and dementia, including Alzheimer’s disease.

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