GAME CHANGER: Is Long COVID an Endothelial Disease of the Spike Protein which also Infects Monocytes Inducing Accelerated Glycolysis that Mimics Cancer Cachexia?
Are Endothelial Cells SARS-CoV-2 What T-Cells Are To HIV?
Metabolic derangement as a result of byproducts released from adipose tissue, tumor cells, skeletal muscle and liver, leading to clinical endpoints.
MAIN POINT: SPIKE PROTEIN DESTRUCTION OF ENDOTHELIAL CELLS – METABOLIC REPROGRAMMING OF MONOCYTES
One of the most important findings in Long COVID patients is that Spike Protein S1 Sub Units persist in Monocytes for up to 15 months post infection.
A statistically significant number of non-classical monocytes contained SARS-CoV-2 S1 protein in both severe (P=0.004) and PASC patients (P=0.02) out to 15 months post-infection.
Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) up to 15 Months Post-Infection
Also, this very same subunit metabolically reprograms monocytes inducing accelerated glycolysis.
A hallmark of COVID-19 is a hyperinflammatory state associated with severity. Monocytes undergo metabolic reprogramming and produce inflammatory cytokines when stimulated with SARS-CoV-2. We hypothesized that binding by the viral spike protein mediates this effect, and that drugs which regulate immunometabolism could inhibit the inflammatory response. Monocytes stimulated with recombinant SARS-CoV-2 spike protein subunit 1 showed a dose-dependent increase in glycolytic metabolism associated with production of pro-inflammatory cytokines.
Metformin Suppresses Monocyte Immunometabolic Activation by SARS-CoV-2 Spike Protein Subunit 1
The Spike Protein invades the Endothelium and damages Endothelial cells.
In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.
SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2
So, we have two separate factors that can induce cancer cachexia, without the presence of cancer. We have endothelial dysfunction on the one hand:
We therefore hypothesized that endothelial dysfunction in the skeletal muscle results in the development of cachexia in cancer.
Abstract 2595: Cancer cachexia is mediated by the suppression of PGC1-alpha expression in the skeletal muscle vasculature
And we have reprogrammed monocytes on the other. BOTH are induced by the Spike Protein.
The reprogrammed monocytes precisely mimic what cancer does to induce cachexia.
Cancer cells affect host metabolism in two ways: (a) their own metabolism of nutrients into other metabolites and (b) circulating factors they secrete or induce the host to secrete. Accelerated glycolysis and lactate production, i.e., the Warburg effect and the resultant increase in Cori cycle activity, are the most widely discussed metabolic effects. Meanwhile, although a large number of pro-cachexia circulating factors have been found, such as TNFa, IL-6, myostatin, and PTHrp, none have been shown to be a dominant factor that can be targeted singly to treat cancer cachexia in humans.
Metabolic Changes During Cancer Cachexia Pathogenesis
As HIV progressively destroys T-cells, is the Spike Protein doing the same to Endothelial Cells?
Our findings show the presence of viral elements within endothelial cells and an accumulation of inflammatory cells, with evidence of endothelial and inflammatory cell death.
Endothelial cell infection and endotheliitis in COVID-19
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Sounds accurate to me. I have long covid and have lost 65 lbs UNINTENTIONALLY since my illness and my body is wasting away. Doctors have tested for cancers and CT scans have been clear and lab work is apparently good. They can’t find a single thing wrong with me. I’m terrified- I don’t know who to turn to for help. I have also suffered from brain fog ever since as well. Unvaccinated thank goodness. I take NAC, Quercetin Zinc and Vitamin D. Not sure what else to do.
Wonderfully articulated and explained, Walter. Thank you so much. I’m off to dinner out in a little while. This will be great dinner conversation because my date (my husband haha) loves to hear me talk about what I learned here and discuss it.