Unravelling shared mechanisms: insights from recent ME/CFS research to illuminate long COVID pathologies

Annesley, Missailidi, Heng, Josev, Armstrong

Approximately half of patients with long COVID (LC) fulfil the diagnostic criteria for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The two conditions share clinical similarities and proposed disease pathologies, but it is still unclear whether they also share common molecular abnormalities.

Most consistently altered pathologies in ME/CFS and LC include an increased reliance on alternatives to carbohydrates as substrates for energy production and altered gut microbiota, with a reduction in butyrate-synthesising bacteria.

Therapeutic approaches targeted at the autoimmune response showed early promising results, but have not passed further clinical trials.

ME/CFS and LC research has identified potential biomarkers, which need to be replicated and validated, with the most accurate and clinically practicable appearing to be measurements of RNAs for ME/CFS.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic illness often triggered by an initiating acute event, mainly viral infections.

The transition from acute to chronic disease remains unknown, but interest in this phenomenon has escalated since the COVID-19 pandemic and the post-COVID-19 illness, termed ‘long COVID’ (LC).

Both ME/CFS and LC share many clinical similarities. Here, we present recent findings in ME/CFS research focussing on proposed disease pathologies shared with LC.

Understanding these disease pathologies and how they influence each other is key to developing effective therapeutics and diagnostic tests.

Given that ME/CFS typically has a longer disease duration compared with LC, with symptoms and pathologies evolving over time, ME/CFS may provide insights into the future progression of LC.

Source: Trends in Molecular Medicine with pdf to full text

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