Underscoring SARS-CoV-2 and SPED (Spike Protein Endothelial Disease): Autopsies Confirm Angiocentric Disease
Asymptomatic infection does not mean harmless – far from it: A continuum of hyperaccelerated aging.
A little over two years ago, on November 20th, 2021, I designed the above graphic and published a post showing proof of how the Spike Protein of SARS-CoV-2 induces all nine Hallmarks of Aging. A recent study has underscored this finding (among dozens and dozens) and brings me pause. The world seems to equate “asymptomatic” and “mild course” with “harmless.” As I have repeatedly warned, this is a very dangerous and ignorant view to hold. Damage is being done. Repeatedly. Just like (again, as I have stated multiple times) the battering ram GROND in the LOTR.
I would like to discuss the problem in action and emphasize the need to continue to find therapeutics to combat these effects. My greatest fear is that we are simply plugging holes in a dam destined to break.
A paper was published about two weeks ago which focused on COVID-19 in children. The finding is consistent with precisely what I have said from Day One. The issue we face is not a “respiratory virus” but a viral protein (Spike Protein) which causes critical endothelial injury and damage.
The common finding of all of the examined COVID-19 cases is the involvement of the endothelium in microcirculation vessels, which are considered to be a primary target of various pathogenic influencing factors. We also discuss both the significance of apoptosis as a result of virus–host interactions and the most likely cause of endothelium cell destruction.
In particular, the findings focused on apoptosis.
According to the obtained data and the literature analysis, the vascular factor can be considered the key factor in COVID-19 pathogenesis. According to Tsankov, COVID-19 should be considered “an angiocentric disease”. The endothelium of microcirculation vessels is the primary and predominating target of the pathogenic influence of various factors. This fact can be confirmed by the presence of SARS-CoV-2 antigens (nucleocapsid protein) as a result of the penetration and replication of the virus in these cells and the further destruction of the infected endothelium cells due to induced apoptosis. Taking into account the unique role of the endothelium, its destruction and subsequent microcirculation disorder are the central points of the development of a capillary–alveolar block, tissue hypoxia, and disseminated intravascular coagulation syndrome (DIC-syndrome), leading to the development of multiple organ dysfunction syndrome (MODS) and, ultimately, death.
We found a significant expression of the apoptosis marker CD95 in the bronchial epithelia, the endothelia of vessels of different sizes, and the macrophages in Patients 1 and 2 (identified on the 6th and 20th days of the disease, respectively). Moreover, a positive reaction with antibodies of CD95 was observed in the apoptosis corpuscles, which simplified their identification. In contrast to Patient 1, apoptosis corpuscles in Patient 2 were identified in a more considerable number and were found everywhere in the bronchi, the direction of the capillaries in the interalveolar septa, the lumen of the alveoli, and the cytoplasm of the macrophages. We found that the localizations of the SARS-CoV-2 neocapsid protein, the apoptosis marker CD95, and the apoptosis corpuscles in different structures of the lungs probably are fundamentally significant in terms of understanding COVID-19 pathogenesis.
I am disturbed that the authors of the paper declare in the conclusion that the N Protein is at fault – when earlier in the paper they clearly state that the S Protein was the one found in macrophages and no staining for the S Protein…
According to the literature data, spike protein expression in the macrophages was noticed in the lungs of a 2-month-old patient who died due to this infection, and the expression of the SARS-CoV-2 S-protein was identified in the macrophages of the lungs of four adults.
COVID-19 in Children: Molecular Profile and Pathological Features
And the Spike has been absolutely proven to damage the Endothelium.
SARS-CoV-2 Spike Protein Binds to Heart’s Vascular Cells Potentially Contributing to Severe Microvascular Damage
Yet, we seem to be missing a very important consideration. The damage to the endothelium of ALL is causing the endothelium to age with each and every infection.
Thus we propose that age-related upregulation of TNFα and caspase 9 and decreased bioavailability of NO promote endothelial apoptosis in coronary arteries that may lead to impaired endothelial function and ischemic heart disease in the elderly.
Proinflammatory phenotype of coronary arteries promotes endothelial apoptosis in aging
And so, we BECOME the elderly, regardless of our current age.
Study after study and paper after paper shows conclusively that those with age-related diseases fare worse with COVID infection/Spike Protein exposure. But, don’t we understand the implication?
Think of it as a conveyer belt. The well are made older, the older are made older still. Each continually moving along the conveyer belt of accelerated aging. We need studies assessing endothelial health in the general population. This is yet another mechanism behind all of the Sudden Cardiac Deaths.
I will continue to work on understanding and solutions.
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