Long COVID could become a widespread post-pandemic disease? A debate on the organs most affected 2023 Ferrara et al

[Andy]

Abstract

Long COVID is an emerging problem in the current health care scenario. It is a syndrome with common symptoms of shortness of breath, fatigue, cognitive dysfunction, and other conditions that have a high impact on daily life. They are fluctuating or relapsing states that occur in patients with a history of SARS-CoV-2 infection for at least 2 months. They are usually conditions that at 3 months after onset cannot be explained by an alternative diagnosis. Currently very little is known about this syndrome.

A thorough review of the literature highlights that the cause is attributable to deposits of tau protein. Massive phosphorylation of tau protein in response to SARS-CoV-2 infection occurred in brain samples from autopsies of people previously affected with COVID-19. The neurological disorders resulting from this clinical condition are termed tauopathies and can give different pathological symptoms depending on the involved anatomical region of the brain. Peripheral small-fiber neuropathies are also evident among patients with Long COVID leading to fatigue, which is the main symptom of this syndrome.

Certainly more research studies could confirm the association between tau protein and Long COVID by defining the main role of tau protein as a biomarker for the diagnosis of this syndrome that is widespread in the post-pandemic period.

Open access, https://link.springer.com/article/10.1007/s00210-023-02417-5

 

[SNT Gatchaman]

This study aims to demonstrate how Long COVID phenomena can be caused by the development of tau protein causing a variety of disorders at various levels in tissues and organs.

Nope.

 

[Creekside]

This hypothesis fails my test for ME: if the symptoms are due to deposits, it doesn't fit the rapidity of switching from full ME to full non-ME that I've experienced. Since Long Covid and ME have similar sets of symptoms, they likely share a common mechanism ... and it's unlikely to be protein deposits.

 

[RedFox]

This hypothesis fails my test for ME: if the symptoms are due to deposits, it doesn't fit the rapidity of switching from full ME to full non-ME that I've experienced. Since Long Covid and ME have similar sets of symptoms, they likely share a common mechanism ... and it's unlikely to be protein deposits.

I like your critical eye. I evaluate ME hypotheses with a similar yardstick: Could they explain PEM? Very few researchers have even tried to. One of the few that tries is hypersensitive microglia, with the additional advantage of proposing an explanation of physical and mental PEM. We're very early in the process of unraveling this illness but currently my money's on low-grade neuroinflammation.

 

[Kitty]

This hypothesis fails my test for ME: if the symptoms are due to deposits, it doesn't fit the rapidity of switching from full ME to full non-ME that I've experienced.

Indeed. Or, I guess, of those who know the exact day on which they transitioned from being a fit and well person with a common viral infection to a chronically ill person.

What struck me about the title was the word "could". Is it not already a worryingly widespread post-pandemic disease?

 

[rvallee]

What struck me about the title was the word "could". Is it not already a worryingly widespread post-pandemic disease?

Yes but admitting so creates legal obligations. Which is a giant loophole when you think of it for more than a second. You can literally fit tens of millions of lives in this loophole. Also the entire psychosomatic pseudoscientific industry gobbling billions while producing nothing at all for it.

 

[Creekside]

Or, I guess, of those who know the exact day on which they transitioned from being a fit and well person with a common viral infection to a chronically ill person.

I was basing it on the 6+ temporary remissions I experienced, where I switched from full ME to full non-ME over the space of < 1 hr. That was from at least three different chemicals (prednisone, cuminaldehyde, T2), and it's unlikely that these three chemicals would affect tau protein deposits in what seemed like identical manners (except that prednisone took 5 days to trigger the switch).