An Approach To Treating Patients With Severe COVID-19 Infection

[md_a]

Patients with COVID-19 infection are at risk of acute respiratory disease syndrome (ARDS) and death. The tissue receptor for COVID-19 is ACE2, and higher levels of ACE2 can protect against ARDS. Angiotensin receptor blockers and statins upregulate ACE2. Clinical trials are needed to determine whether this drug combination might be used to treat patients with severe COVID-19 infection.


An approach to treating patients with severe COVID-19 infection might be hiding in plain sight. The tissue receptor for the virus is ACE2, which is also the receptor for the SARS coronavirus (1). Several years ago, investigators in the Netherlands and elsewhere showed that ARBs and statins upregulate the activity of ACE2 (14, 15), and higher levels of ACE2 are associated with a reduced severity of ARDS (16). Both statins and ARBs target the host response to infection, not the virus (9). They act largely (although not exclusively) on endothelial dysfunction, which is a common feature of many virus infections (17). Both drugs counter endothelial dysfunction by affecting the ACE2/angiotensin-(1–7)/Mas and angiopoietin/Tie-2 signaling axes (9).


Hiding in Plain Sight: an Approach to Treating Patients with Severe COVID-19 Infection

 

[LeeLemonoil]

Why would upregulating of the receptor the virus enters the cells in the first place be helpful? Sounds like the contrary is true.

Then, it’s unclear if that is the only way the virus enters cells. Spike Proteins are involved and the virus ability to „open“ tissue by divulging it via Proteases.
Viruses adapt. Host conditions differ. Virus will enter where he can. I think we see differences in lethality because the virus adapted to different ways to enter cells.

Look at the many old nursing home dead.

They are all on statins and Ace-inhibitors. That either is directly dangerous because the virus enters via Ace2-more easily or it is like the study sais and the virus has problems entering that way. And in the old and infirm has time and opportunity to adapt/mutate and enter via different ways, maybe his proteases become more aggressive.

That mutation of virus might be more dangerous to younger and healthier people too, thus so many dead in Italy and Madrid

 

[Xemnoraq]

Why would upregulating of the receptor the virus enters the cells in the first place be helpful? Sounds like the contrary is true.

Then, it’s unclear if that is the only way the virus enters cells. Spike Proteins are involved and the virus ability to „open“ tissue by divulging it via Proteases.
Viruses adapt. Host conditions differ. Virus will enter where he can. I think we see differences in lethality because the virus adapted to different ways to enter cells.

Look at the many old nursing home dead.

They are all on statins and Ace-inhibitors. That either is directly dangerous because the virus enters via Ace2-more easily or it is like the study sais and the virus has problems entering that way. And in the old and infirm has time and opportunity to adapt/mutate and enter via different ways, maybe his proteases become more aggressive.

That mutation of virus might be more dangerous to younger and healthier people too, thus so many dead in Italy and Madrid

Those are some good points, its actually Ray that suggested this approach to promoting ace2 and inhibiting angiotensin, however if i remember correctly i think its ace1 that promotes angiotensin and ace2 that degrades it, so which one do the ace inhibitors act on number one or two?

Im not 100% sure about what i mentioned on ace1 just going off of what i remember hearing Ray say, i think he mentioned ace1 actually promotes angiotensin, i could be wrong though

 

[meatbag]

Those are some good points, its actually Ray that suggested this approach to promoting ace2 and inhibiting angiotensin, however if i remember correctly i think its ace1 that promotes angiotensin and ace2 that degrades it, so which one do the ace inhibitors act on number one or two?

Im not 100% sure about what i mentioned on ace1 just going off of what i remember hearing Ray say, i think he mentioned ace1 actually promotes angiotensin, i could be wrong though

ACE1 makes angiotensin and ACE2 degrades it.

Yeah, Peat said the virus binds to the ACE2 enzyme and enters the cell through the type 1 angiotensin-2 (AT-1) receptor

 

[Xemnoraq]

ACE1 makes angiotensin and ACE2 degrades it.

Yeah, Peat said the virus binds to the ACE2 enzyme and enters the cell through the type 1 angiotensin-2 (AT-1) receptor

ok right on i thought so! so maybe the ace inhibiting drugs inhibit ace 2?

 

[RWilly]

Here's an excellent explanation of ACE2. Starts at about the 40 second mark: