April 2, 2022

A paper published online Thursday directly contradicts claims that “COVID infection is more likely to cause Myocarditis. Please read this key finding in the paper:

In influenza, viral binding to host cells induces a type I and III interferon response, including inflammatory cytokines (IL-6, TNF-α) and chemokines. The binding of the type I and III IFNs to their receptors results in activation of the JAK/STAT pathways for the induction of ISGs such as IFI. This can lead to acute myocarditis, a common complication of influenza infection63. In contrast to influenza infection, induction of these pathways in COVID-19 is low, a feature supported by recent autopsy studies in which virus was not detected as a cause of myocarditis.

If we look to research from last year, we find that SARS-CoV-2 reduces cardiomyocyte contractility through sarcomere breakdown and cardiomyocyte cell death.

But what is this? This is exactly the same process that occurs in Cardiac Amyloidosis – and it can happen very quickly.

A fundamental question in protein aggregate pathologies across multiple organ systems is whether protein aggregates are “good” or “bad” (Cox et al., 2018). When viewed as part of the static sarcomere model, protein aggregates have always been regarded as a pathologic, potentially toxic entity (Henning and Brundel, 2017). Indeed, akin to the pathology observed in neurodegenerative diseases, both pre-amyloid oligomers (Del Monte and Agnetti, 2014) and protein aggregates, consisting of a combination of normal sarcomeric proteins with or without mutated proteins, have been ascribed toxic roles. This notion is reinforced by studies that show that intracytoplasmic accumulation of these pre-amyloid oligomers, aggregates or their “toxic” constituents, recapitulates cardiotoxicity (Sanbe et al., 2004; Pattison et al., 2008, 2011); akin to a toxic role for pre-amyloid Aβ oligomers postulated as a pathogenic mechanism in Alzheimer’s disease.

Another finding of the paper from Thursday, Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage, shows a DNA damage response parallel to the DNA damage response of Alzheimer’s. What is most interesting about this? THE SAME ALTERED DNA REPAIR PATHOGENIC PATHWAY APPLIES TO THE OBESE!

Unrepaired DNA double-strand breaks (DSBs) are lethal. The typical pathological hallmarks of Alzheimer’s disease include accumulation of β-amyloid, tau hyperphosphorylation, synaptic damage, and cell death. Nevertheless, heterogeneity in Alzheimer’s populations, and failure of β-amyloid-targeted drug trials signal a need to investigate alternative targetable-pathways that may occur upstream in the disease process. Several new lines of evidence indicate a bidirectional relationship between these common pathological changes observed in Alzheimer’s disease, and DNA damage.

The Thursday paper also showed altered transcriptomics with genes associated with heat shock – another hallmark in Cardiac Amyloidosis. A class of heat shock proteins exist in bacterial, fungal and plant systems, i.e., the Hsp110 AAA + ATPase disaggregases that can disassemble amyloid and protein aggregates (Torrente and Shorter, 2013). Recent studies indicate that proteins with disaggregase function (some with Hsp homology) exist in the animal kingdom but their role appears to be unclear. The dysregulation of these proteins allows for the rapid onset and progression of Cardiac Amyloidosis.

And this ties into precisely what we are seeing, including hearts that weigh over 500g. Cardiac amyloid deposition is most common in the myocardium but is also seen in the atria, pericardium, endocardium, and vasculature. The myocardium becomes thick (mean weight 500 g) with a rubbery consistency. High-grade infiltration (>50%) of myocardium is most common in the AL variety, and 90% of cases have vascular involvement. Epicardial vessels are typically spared, but microvascular involvement is common, resulting in tissue ischemia and infarction. Resultant myocardial fibrosis adds to the myocardial dysfunction, causing heart failure and cardiac arrhythmias.

I believe this offers further evidence that the Spike Protein of SARS-CoV-2 is perhaps the most dangerous pathogen to ever appear on the planet. And yet, nobody with any control over public health is willing to do anything about it.

Referenced/Related Papers

Come Together: Protein Assemblies, Aggregates and the Sarcostat at the Heart of Cardiac Myocyte Homeostasis

SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis

Altered DNA repair; an early pathogenic pathway in Alzheimer’s disease and obesity

Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage