Nasty Enzyme involved in Covid Severity

Wishful

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https://www.sciencedaily.com/releases/2021/08/210824135358.htm

"Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest University School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme -- secreted phospholipase A2 group IIA, or sPLA2-IIA -- may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.

sPLA2-IIA, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.

When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs,"



That damage to cell membranes sounds like it could account for ME symptoms too. Maybe we are producing too much of this enzyme in response to even mild inflammatory events. Exert a bit, which activates immune cells, which then increases production of this enzyme, which in turn damages cells. My ME responds to different types of fatty acids, which are used to build/repair membranes.

A quick Google didn't show any links for 'sPLA2-IIA me/cfs', so the amount in circulation is something that researchers should check in their patients.
 

SWAlexander

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rattlesnake venom
Having Anti-Phospholipid Syndrome, I try to read everything related.
I even found genetic markers (23andme) for PLA2G2A
I very strongly believe there is a significant component to ME.

Example:
Snake Venom Cytotoxins, Phospholipase A2s, and Zn2+-dependent Metalloproteinases: Mechanisms of Action and Pharmacological Relevance

Abstract

Snake venom toxins are responsible for causing severe pathology and toxicity following envenomation including necrosis, apoptosis, neurotoxicity, myotoxicity, cardiotoxicity, profuse hemorrhage, and disruption of blood homeostasis. Clinically, snake venom toxins therefore represent a significant hazard to snakebite victims which underscores the need to produce more efficient anti-venom. Some snake venom toxins, however, have great potential as drugs for treating human diseases. In this review, we discuss the biochemistry, structure/function, and pathology induced by snake venom toxins on human tissue. We provide a broad overview of cobra venom cytotoxins, catalytically active and inactive phospholipase A2s (PLA2s), and Zn2+-dependent metalloproteinases. We also propose biomedical applications whereby snake venom toxins can be employed for treating human diseases. Cobra venom cytotoxins, for example, may be utilized as anti-cancer agents since they are efficient at destroying certain types of cancer cells including leukemia. Additionally, increasing our understanding of the molecular mechanism(s) by which snake venom PLA2s promote hydrolysis of cell membrane phospholipids can give insight into the underlying biomedical implications for treating autoimmune disorders that are caused by dysregulated endogenous PLA2 activity. Lastly, we provide an exhaustive overview of snake venom Zn2+-dependent metalloproteinases and suggest ways by which these enzymes can be engineered for treating deep vein thrombosis and neurodegenerative disorders.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4060629/
 

Wishful

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I was thinking more about this. Researchers have been looking for major signs of this disease: the equivalent of exploding cars (Pinto!). ME could be more like the equivalent of corrosion in some critical connectors in today's highly-computerized vehicles. Imagine your immune system activating a bit more due to some exertion, increasing the production of these enzymes. They punch a few holes in some cell (or mitochondrial) membranes, increasing or decreasing the flow of molecules or vesicles, making the cells function at less than 100% efficiency. How easy is it to find that sort of damage? Worse, what if that partial damage is happening to brain cells in just some parts of the brain?
 

SWAlexander

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"Worse, what if that partial damage is happening to brain cells in just some parts of the brain?"
This was my biggest concern.
Now, as thrombosis begins to disappear my short-term memory is coming (slowly) back.
if blood flow is interrupted by thrombosis no oxidant and sugar can reach the brain.
Thrombosis creates the same disaster in pulmonary embolism as result.
At the end, when blood clots keep depriving nutrients and minerals of reaching their destiny, the cell nucleus will die.
Hypercoagulable states or Anti-Phospholipid Syndrome
 

wastwater

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Low complement c3 does this,I suspect I have inherited mine
In addition to studying C3 deficiency in diagnosed human patients, researchers have studied C3 deficiency in animals. C3 deficiency can be induced by injecting animals with cobra venom factor, which functions like an unregulated C3-convertase because factor I and factor H do not regulate it, cleaving most C3 molecules in the serum into C3a and C3b fragments, which depletes the amount of intact C3.[4]
https://en.m.wikipedia.org/wiki/Complement_3_deficiency
 
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