How The Coronavirus Infects Human Cells | Dr. David Seaman

The tale Covid that rose in late 2019 called SARS-CoV-2 enters cells by authoritative to a catalyst called angiotensin changing over chemical 2 (ACE2). I have seen that this protein is alluded to by numerous individuals as the ACE2 receptor. You ought to comprehend that ACE2 isn't a receptor, it is a chemical. The essential capacity of ACE2 is to change over a favorable to provocative substance called angiotensin II into mitigating angiotensin-(1-7).

Angiotensin II builds pulse and furthermore advances aggravation and lung harm, which is checked by angiotensin-(1-7), which implies we have to create a satisfactory measure of angiotensin-(1-7) to adjust the impacts of angiotensin II. This happens in sound individuals, in which an equalization is struck between angiotensin II and angiotensin-(1-7) by the activities of ACE2. Sadly, factor degrees of ACE2 inadequacy are found in the older populace, just as in individuals with diabetes, hypertension, and coronary illness. These are similar individuals at a more serious danger for a helpless result whenever tainted by SARS-CoV-2 (1).

It ought to be perceived that diabetes, hypertension and coronary illness quite often share a typical issue, that being raised blood glucose levels. The metabolic condition is a hyperglycemic state (high blood glucose levels), which prompts the improvement of diabetes, hypertension, coronary illness, and most other constant maladies.

An excess of glucose available for use prompts a cycle called glycosylation, wherein proteins become "glossed over." You may have known about hemoglobin A1c, which is likewise alluded to as glycosylated hemoglobin. For all intents and purposes this implies hemoglobin in red platelets gets "glossed over." Hemoglobin A1c is the most regularly measure glycosylated protein. Things being what they are, ACE2 can likewise become glycosylated, which seems to expand the capacity of SARS-CoV-2 to taint lung cells (2).

When a lung cell is contaminated by SARS-CoV-2, there is a further decrease of ACE2 movement, which further amplifies the lopsidedness between lung harming angiotensin II and lung defensive angiotensin-(1-7). This assists with clarifying why individuals with hyperglycemia (diabetes, hypertension, and coronary illness) are at a more serious danger for building up an extreme instance of COVID-19 (1,2). The Covid all the more effectively accesses lung cells because of the glycosylation of ACE2, and once contaminated there is a more prominent decrease in ACE2 movement, which improves the favorable to fiery unevenness between angtiotensin II and angiotensin-(1-7). Watch the following video to see how this process works:



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