Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis, 2021, Sfera et al

Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive.

With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers.

Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.

Open access, https://www.frontiersin.org/articles/10.3389/fncel.2021.673217/full

 

It is an interesting hypothesis, but is very much of house-of-cards construction, requiring a lot of empirical validation steps that could easily turn out not to be true.

I do note they've singled out a few things that I have previously talked about in my random/speculative ideas thread, that no ME/CFS researchers have been interested in so far (NRP).

 

"With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus." . if they do not even take note of the major symptoms and write everthing of as chronic tiredness they cannot be taken seriously as researchers .

 

Well, this is pretty close to what has been my leading pet "guess" for a while - except for attributing the translocation to "endothelial senescence."

I haven't read the paper yet, but it does seem like a hypothesis based upon another hypothesis; though they say, "This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide." It will be interesting to see exactly how the model is supported.

If nothing else, I hope they get the chance to test their hypotheses and that this doesn't just fall by the wayside.

 

Reminds me of Derya Unutmaz work on MAIT cells in the gut lining - not sure what became of that

Also, James Baraniuk patented an idea that leaky junctions in the blood brain barrier were relevant.

@Andy posted a link to a study which looked at LPS recently (last week?)

EDIT - there's been a fair bit on endothelia dysfunction over the years