This video is a summary of all the autopsy findings that have been done on coronavirus patients. This is based on 8 published studies and/or case reports. Here are the links to those studies:
SARS-CoV-2 exhibits selectivity for the lungs. Specifically, type II pneumocytes, meaning type II alveolar cells. Alveoli are the tiny microscopic air sacs of the lungs, which is the part of our lungs that is responsible for gas exchange. Air is brought down into the lungs, to the alveoli, and the oxygen diffuses from the alveoli into our tiny blood vessels there, called capillaries. At the same time, carbon dioxide, a waste product from our body, travels from the capillaries into our alveoli, and we then exhale out that carbon dioxide. Alveoli are made up of mainly type I alveolar cells. But to a lesser degree, they are also made up of type II alveolar cells, and these guys are sort of like the maintenance guys for the alveoli. They play a part in making surfactant, a sort of lubricant for the alveoli. But these cells also play a part in defending against foreign pathogens, like viruses and bacteria.
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Well as it turns out these type II alveolar cells have the ACE2 receptors on them, and SARS-CoV-2 binds to this receptor, and that’s how it gains entry into these cells, and into our body. When the SARS-CoV-2 invades the type II alveolar cells, it precipitates a cascade of reactions that causes the body to react to it, with inflammation, and lots of damage to the alveoli, known as diffuse alveolar damage. Clinically, this is what we call ARDS, acute respiratory distress syndrome. This is what causes oxygen levels to go down, and what causes the so-called cytokine storm. When people die of COVID, this is what’s going. Also, there is a propensity for blood clots to develop, and some people with COVID died as a result of pulmonary emboli, meaning blood clots in their lungs. The capillaries in the lung surround the alveoli. Here, they serve to bring red blood cells in close proximity to the alveoli, to allow gas exchange to occur, like I mentioned earlier. The lining of these capillaries is called the endothelium, the cells that make up the endothelium here, also have ACE2 receptors. The virus, at least in those with severe disease, seems to be infiltrating the endothelium and causing inflammation and injury to the capillaries, not just the alveoli. This likely at least partially explains why this virus is causing blood clots to develop here.
So we are seeing a common theme here, and that is microthrombi that are being found in blood vessels of pretty much all the organs, including brain, kidneys, heart, liver, and of course lungs. This is likely all because of endothelial damage that occurs as a result of the virus binding to the ACE2 receptors that are located there.
After all, in some of these autopsy studies, they used electron microscopy to find what appeared to be viral particles in the endothelial cells not only in the lungs, but also in the heart and kidneys.The endothelial damage serves to trigger the clotting process, something known as a coagulation cascade. But its also possible that the endothelial damage is mainly occurring in the lung capillaries, and that’s where the tiny clots first develop, and then they end up traveling to other parts of the body, eventually lodging in blood vessels of other organs. Or it could be both of these things. It’s interesting to note that Endothelial cells are more vulnerable to dying in people with preexisting endothelial dysfunction, which is more often associated with being a male, being a smoker, having high blood pressure, diabetes, and obesity. So overall, organ damage that occurs in severe COVID is likely a result of a multitude of factors, such as:
1) Directly viral invasion by means of the ACE2 receptor
2) Indirect damage that occurs as a result of cytokine storm
3) Indirect damage by means of blood clots
4) Indirect damage that occurs as a result of oxygen deprivation, as well as toxic effects of various drug treatments, and other factors as well