Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases 2023 Peterson, Roy et al

Abstract

Historically, COVID-19 emerges as one of the most devastating diseases of humankind, which creates an unmanageable health crisis worldwide. Until now, this disease costs millions of lives and continues to paralyze human civilization's economy and social growth, leaving an enduring damage that will take an exceptionally long time to repair. While a majority of infected patients survive after mild to moderate reactions after two to six weeks, a growing population of patients suffers for months with severe and prolonged symptoms of fatigue, depression, and anxiety. These patients are no less than 10% of total COVID-19 infected individuals with distinctive chronic clinical symptomatology, collectively termed post-acute sequelae of COVID-19 (PASC) or more commonly long-haul COVID. Interestingly, Long-haul COVID and many debilitating viral diseases display a similar range of clinical symptoms of muscle fatigue, dizziness, depression, and chronic inflammation.

In our current hypothesis-driven review article, we attempt to discuss the molecular mechanism of muscle fatigue in long-haul COVID, and other viral diseases as caused by HHV6, Powassan, Epstein–Barr virus (EBV), and HIV. We also discuss the pathological resemblance of virus-triggered muscle fatigue with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Open access, https://infectagentscancer.biomedcentral.com/articles/10.1186/s13027-023-00485-z

 

I wish they would clarify the depression is situational ie a downstream effect of having your life suddenly altered for the worse . as for anxiety does that word have any clear meaning to anyone .

 

This hypothesis paper spends time talking about demyelination and muscle infiltration by cytotoxic CD8+ Ts as an explanation of long-term muscle fatigue. This doesn't ring true to me. My muscle power can be relatively normal one day and poor another, while general co-ordination is only (a bit) affected by effector power rather than input control (as I perceive it). I don't think such rapid symptom changes comport with mechanisms like those being suggested.

Leaving aside the odd case report of overt demyelinating lesions in LC, is there much evidence of demyelination in ME/CFS? I note this relatively recent thread which quoted back to 2003 —

To my mind, the tiny ("punctate") T2/FLAIR hyperintensities are more likely to represent abnormally enlarged perivascular spaces, relating to BBB damage +/- associated regional immune cell infiltration.

I much preferred this group's prior focus on mitochondrial dysfunction, autophagy/mitophagy etc.

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A Comparison of Neuroimaging Abnormalities in Multiple Sclerosis, Major Depression and Chronic Fatigue Syndrome (Myalgic Encephalomyelitis): is There a Common Cause? (2018)

 

My test for ME hypotheses is: "Does this fit with the rapid complete temporary remissions I experienced?" If the hypothesized mechanism doesn't allow a complete switch from full ME to full non-ME in less than an hour, I give it a failing grade.