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05-01-2020 03:12 AM (Last edited 05-01-2020 04:48 AM ) in
Tech TalkEvidence for it's effects and widespread of the covid.
Read the Article:
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltextQuora Link to the same:
Translation
( What is the importance of knowing it infects endothelial cells?)
Endothelial cells are found all over the body, in every organ. They also line blood vessels. We have seen clinically that COVID affects clotting, as there have been a number of cases of both strokes and pulmonary emboli seen in these patients.
If the virus is infecting the endothelial cells, it could explain the widespread effects we are seeing on the vascular system. Endothelial inflammation can stimulate blood clot formation.
It may also help explain why the effects of the virus are so widespread. We have seen COVID effect prety much every body system, which is not typical for a viral infection.
Conclusion:
In conclusion, we might need ACE2 based treatment approaches together with natural antiinflammatory antioxidants to limit aberrant vascular responses and arterial thrombosis associated with what has come to be called Covid 19 Associated Coagulopathy in patients with corona viremia.
Physiologically ACE2 converts Angiotensin II to Angiotensin 1-7. Angiotensin 1-7 is both a vasodilator and an anti-inflammatory agent. It also limits and attenuates the production of reactive oxygen species by vascular endothelial cells. It functions to improve endothelial homeostasis through a mechanism that involves attenuation of NADPH oxidase induced reactive oxygen species production. Reactive oxygen species such as superoxide can kill/destroy cells very quickly. Remember it is used by neutrophils to kill bacteria. There is a version of the same NADPH oxidase in vascular endothelial cells. ACE2 confers endothelial protection and attenuates atherosclerosis.
Remember that the ACE2 receptor is used by the coronavirus for binding and entry into epithelial cells in the upper, lower respiratory tract, and vascular endothelial cells. But binding of the coronavirus knocks out the ACE2 enzyme.
As a result, when the ACE2 on vascular endothelial cells is knocked out by the Coronavirus, NADPH oxidase reign without any restrain to increase reactive oxygen species production because there's no Angiotensin 1-7. This causes injury and the destruction of endothelial cells.
ENDOTHELIAL INFLAMMATION FOLLOWS DAMAGE TO THE ENDOTHELIAL CELLS. VWF is released from the subendothelial cells following damage to vascular endothelial cells by the coronavirus. With the inflammatory response that follows, VWF coupled with factor 8 forms intraarterial thrombosis.
Therefore, Vasoconstriction, increased blood pressure, increased vascular permeability, pulmonary edema, and Respiratory distress automatically follows the binding of the Coronavirus to ACE2 on vascular endothelial cells. This occurs because ACE2 is needed to downregulate Angiotensin II. But when the coronavirus binds to ACE2 it knocks it off causing vasoconstricting Angiotensin II LEVELS that causes oxidative stress, increased blood pressure, increased vascular permeability, and Respiratory distress.
ACE2 KNOCK OUT ON VASCULAR ENDOTHELIAL CELLS
The ACE2 Knock out by the Coronavirus during the viremic phase, therefore, allows unopposed Angiotensin II to reign supreme to cause more vasoconstriction, oxidative stress, increased vascular permeability, the release of Von Willebrand factor clot formation, clot lysis and increase in d-Dimer.
This occurs when Viraemia sets in. A good defense mechanism will block the passage from the respiratory tract to the bloodstream.
*Everything is from Quora
-by Trumalai Kamala , immunologist, Ph.D Mycobacteriology
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