A Universal “AIDS”

SARS-CoV-2, the Spike Protein, and the Slow, Progressive Destruction of Infected Cells

I dedicate this post to the memory of Luc Montagnier. 

AIDS is known as Acquired Immune Deficiency Syndrome because of the EFFECT of the HIV virus, not because of what the virus DOES. The HIV virus, which causes AIDS, destroys the cells which it infects. The virus infects CD4 T-Cells. Over time, when the number of CD4 T-Cells reaches a low enough number, the body can no longer defend itself and AIDS sets in. HIV does not cause your immune system to malfunction on a systemic level. HIV slowly destroys one of the critical components of your immune system, causing it to fail. 

Now, what type of cell a virus infects is called Tropism. The HIV virus infects CD4 T-Cells. The SARS-CoV-2 2 virus and its Spike Protein infect virtually EVERY cell. 

Do you understand what is happening? This explains EVERYTHING! 

Based upon the Spike Protein’s tropism. let us look at what happens when we have the slow, progressive destruction of different cell types. 

CARDIOMYOCYTES 

Loss of cardiomyocytes plays a critical role in the pathogenesis of heart failure. With fewer myocytes, the heart is unable to sustain efficient contraction. Much attention has been focused on understanding mechanisms of cell death in myocytes with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Both necrosis and apoptosis contribute to loss of myocytes, and this loss of cells is a hallmark of cardiac pathologies, including ischemia/reperfusion, myocardial infarction, and heart failure. Apoptosis is a highly regulated process that is activated via death receptors in the plasma membrane or via permeabilization of the mitochondria. Necrosis is generally viewed as an uncontrolled process that leads to mitochondrial swelling, cell rupture, and subsequent inflammation. 

Cell Death in the Myocardium: My Heart Won’t Go On 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074399/ 

NEURONAL CELLS 

Neurodegeneration is a slow and progressive loss of neuronal cells in specified regions of the brain and is the main pathologic feature of Alzheimer’s disease, Parkinson’s disease, etc. The underlying pathophysiology of these neurodegenerative diseases is oxidative stress from impaired mitochondrial function, deposition of aggregated proteins, neuroinflammation, and activation of apoptotic factors. 

Quercetin and antioxidant potential in diabetes 
Francis I. Achike, Dharmani D. Murugan, in Diabetes (Second Edition), 2020 

PANCREATIC BETA CELLS 

Beta cell insults include cytokine-induced inflammation, obesity and insulin resistance, and overconsumption of saturated fat and free fatty acids (FFA). A progressive decline of beta cell function leading to beta cell exhaustion precedes beta cell demise (Ferrannini, 2010; Talchai et al., 2012). Loss of beta cell mass and function are central to the development of both type 1 and 2 diabetes (Stoffers, 2004). 

Beta Cell Dysfunction and Insulin Resistance 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3608918/ 

MUSCLE CELLS 

Sarcopenia is the age-related progressive loss of muscle mass and strength. The main symptom of the condition is muscle weakness. Sarcopenia is a type of muscle atrophy primarily caused by the natural aging process. Scientists believe being physically inactive and eating an unhealthy diet can contribute to the disease. 

Sarcopenia 
https://my.clevelandclinic.org/health/diseases/23167-sarcopenia 

ENDOTHELIUM (Why Spike Protein Disease Resembles Graft vs. Host Disease) 

Endothelial Cell Death Contributes to Vascular Remodeling, Autoimmunity and Inflammation 

The presence of dying renal cells in association with AKI or rejection episodes has been known for decades. However, the characterization of molecular pathways controlling regulated renal cell death responses is still an evolving field. Two major types of programmed cell death, apoptosis and necroptosis, have been characterized in association with AKI (23, 26, 65–73), although various death and inflammatory pathways such as ferroptosis and pyroptosis also likely contribute (74–76). 

Endothelial Dysfunction in Kidney Transplantation 
https://www.frontiersin.org/articles/10.3389/fimmu.2018.01130/full 

Now do you see what is happening? 

JUST AS AIDS IS THE EFFECT OF HIV’S DESTRUCTION OF CD4 T-CELLS, ALL THE PATHOLOGIES BEING OBSERVED POST SPIKE PROTEIN EXPOSURE ARE THE EFFECTS OF THE SPIKE PROTEIN’S DESTRUCTION OF VIRTUALLY EVERY CELL TYPE! 

We are dealing with an “AIDS” of universal scope. We need to understand if this virus is acting like HIV and other latent viruses. Is it slowly, inexorably destroying everything it touches? Cell. By. Cell. 

I pray not.