This video is a listing of all of the autopsy findings which have been done on coronavirus patients. This is dependant on 8 printed studies and/or situation reports. Listed here are the hyperlinks to individuals studies:
https://world wide web.acpjournals.org/doi/10.7326/M20-2003
https://world wide web.acpjournals.org/doi/10.7326/M20-2566
https://world wide web.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30243-5/fulltext
https://world wide web.nejm.org/doi/full/10.1056/NEJMoa2015432
https://world wide web.medrxiv.org/content/10.1101/2020.05.18.20099960v1
https://world wide web.nejm.org/doi/full/10.1056/NEJMc2019373
https://world wide web.thelancet.com/journals/lancet/article/PIIS2213-2600(20)30076-X/fulltext
SARS-CoV-2 exhibits selectivity for that lung area. Particularly, type II pneumocytes, meaning type II alveolar cells. Alveoli would be the small microscopic air sacs from the lung area, the a part of our lung area that accounts for gas exchange. Air is introduced lower in to the lung area, towards the alveoli, and also the oxygen diffuses in the alveoli into our small bloodstream vessels there, known as capillaries. Simultaneously, co2, a waste product from your body, travels in the capillaries into our alveoli, so we then exhale out that co2. Alveoli comprise mainly type I alveolar cells. But to some lesser degree, they’re also comprised of type II alveolar cells, which guys are kind of such as the maintenance guys for that alveoli. They play a role for making surfactant, a kind of lubricant for that alveoli. However these cells also play a role in protecting against foreign pathogens, like infections and bacteria.
Well actually these type II alveolar cells possess the ACE2 receptors in it, and SARS-CoV-2 binds for this receptor, and that’s the way it gains entry in to these cells, and into the body. Once the SARS-CoV-2 invades the kind II alveolar cells, it precipitates a cascade of reactions that triggers your body to respond to it, with inflammation, and a lot of harm to the alveoli, referred to as diffuse alveolar damage. Clinically, this is exactly what we call ARDS, acute respiratory system distress syndrome. This is exactly what causes oxygen levels to visit lower, and just what causes the so-known as cytokine storm. When individuals die of COVID, this really is what’s going. Also, there’s a tendency for thrombus to build up, and a few individuals with COVID died because of lung emboli, meaning thrombus within their lung area. The capillaries within the lung surround the alveoli. Here, they actually bring red bloodstream cells in close closeness towards the alveoli, to permit gas exchange to happen, like I pointed out earlier. The liner of those capillaries is known as the endothelium, cells that comprise the endothelium here, also provide ACE2 receptors. Herpes, a minimum of in individuals with severe disease, appears to become infiltrating the endothelium and causing inflammation and injuries towards the capillaries, not only the alveoli. This likely a minimum of partly explains why herpes causes thrombus to build up here.
So there has been a typical theme here, and that’s microthrombi which are being present in bloodstream vessels of practically all the organs, including brain, kidneys, heart, liver, not to mention lung area. This really is likely all due to endothelial damage occurring because of herpes binding towards the ACE2 receptors which are located there.
In the end, in a few of these autopsy studies, they used electron microscopy to locate what made an appearance to become viral particles within the endothelial cells not just in the lung area, but additionally within the heart and kidneys.The endothelial damage serves to trigger the clotting process, something referred to as a coagulation cascade. Nevertheless its also entirely possible that the endothelial damage is principally occurring within the lung capillaries, and this is where the small clots first develop, and they finish up visiting other areas of the body, eventually lodging in bloodstream vessels of other organs. Or it may be these two things. It’s interesting to notice that Endothelial cells tend to be more susceptible to dying in individuals with preexisting endothelial disorder, that is more frequently connected with as being a male, as being a smoker, getting high bloodstream pressure, diabetes, and weight problems. So overall, organ damage occurring in severe COVID is probably a direct result numerous factors, for example:
1) Directly viral invasion by way of the ACE2 receptor
2) Indirect damage occurring because of cytokine storm
3) Indirect damage by way of thrombus
4) Indirect damage occurring because of oxygen deprivation, in addition to toxic results of various prescription drugs, along with other factors too