Also ACE receptor blockers. I'm not a doc, and I'm not suggesting anything. Also, everyone (Doctor organizations) right now recommends continuing your meds, so talk to your doc. Don't take medical advice from anyone on the internet. This is only for discussion/information. I studied biochem and take an ACEi myself, so I'm interested.

SARS-CoV and NL63 (another, less-deadly coronavirus) use the same receptor, angiotensin converting enzyme (ACE)-2, for entry into the host cell. https://www.ncbi.nlm.nih.gov/pubmed/18931070

Another article:

"Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/

Here is a good summary I found, too. http://www.nephjc.com/news/covidace2

If anyone has seen any additional information posted, please share.

God bless and wash your hands.

From the last link posted. If you have hypertension, the outcome appears to be worse:



But these are just raw, early results and not formal studies, adjusted for other factors, etc...

https://www.dicardiology.com/content/esc-council-hypertension-says-ace-i-and-arbs-do-not-increase-covid-19-mortality

there genetic/ethinic correlations? Could certain ethnic groups be higher risk?

We talked about this a bit on Sunday.

https://texags.com/forums/84/topics/3100014

I'm not a physician, but I don't think it appears there's great reason to stop taking these meds. In fact, there appeared to be some experimental evidence that there could be a beneficial effect, if any at all.

SARS uses the ACE2 receptor as an entry point, but there's apparently evidence that ACE2 expression may be down regulated after infection. An absence of ACE2 activity in response to infection may lead to more accumulation of Angiotensin II and make the cardiac complications worse. If ARBs and ACE inhibitors are working to keep AngII levels down, this may not be something you want to stop if ACE2 activity is compromised.

There was also some concern that the drugs have shown evidence of upregulation of ACE2 in rodent studies. It seems counterintuitive to want to have more ACE2 if that's the receptor that is attacked, but the absence of it may work more against you than for you.

Ultimately, a lot of clinical data will be needed to know if these drugs exhibit any effect, good or bad. It at least appears from my reading that the potential for good is more evident, especially considering that these drugs are helping to control something that has a lot better chance of killing you.

The use of ACEI and ARBs would be a poor use at best in trying to prevent infection. The focus should be on modifying protease inhibitors similar to those used in HIV Prep to help combat COVID-19.

I am a hospitalist in North Dallas.
Here is an excellent video describing the use of ACE inhibitors or ARBs in Covid 19.

cisgenderedAggie said:

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We talked about this a bit on Sunday.

https://texags.com/forums/84/topics/3100014

I'm not a physician, but I don't think it appears there's great reason to stop taking these meds. In fact, there appeared to be some experimental evidence that there could be a beneficial effect, if any at all.

SARS uses the ACE2 receptor as an entry point, but there's apparently evidence that ACE2 expression may be down regulated after infection. An absence of ACE2 activity in response to infection may lead to more accumulation of Angiotensin II and make the cardiac complications worse. If ARBs and ACE inhibitors are working to keep AngII levels down, this may not be something you want to stop if ACE2 activity is compromised.

There was also some concern that the drugs have shown evidence of upregulation of ACE2 in rodent studies. It seems counterintuitive to want to have more ACE2 if that's the receptor that is attacked, but the absence of it may work more against you than for you.

Ultimately, a lot of clinical data will be needed to know if these drugs exhibit any effect, good or bad. It at least appears from my reading that the potential for good is more evident, especially considering that these drugs are helping to control something that has a lot better chance of killing you.

---

New literature this evening is actually suggesting that ACE2 expression is increased during viral infection, not decreased (or at least interferon stimulated)

Ranger222 said:

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cisgenderedAggie said:

---

We talked about this a bit on Sunday.

https://texags.com/forums/84/topics/3100014

I'm not a physician, but I don't think it appears there's great reason to stop taking these meds. In fact, there appeared to be some experimental evidence that there could be a beneficial effect, if any at all.

SARS uses the ACE2 receptor as an entry point, but there's apparently evidence that ACE2 expression may be down regulated after infection. An absence of ACE2 activity in response to infection may lead to more accumulation of Angiotensin II and make the cardiac complications worse. If ARBs and ACE inhibitors are working to keep AngII levels down, this may not be something you want to stop if ACE2 activity is compromised.

There was also some concern that the drugs have shown evidence of upregulation of ACE2 in rodent studies. It seems counterintuitive to want to have more ACE2 if that's the receptor that is attacked, but the absence of it may work more against you than for you.

Ultimately, a lot of clinical data will be needed to know if these drugs exhibit any effect, good or bad. It at least appears from my reading that the potential for good is more evident, especially considering that these drugs are helping to control something that has a lot better chance of killing you.

---

New literature this evening is actually suggesting that ACE2 expression is increased during viral infection, not decreased (or at least interferon stimulated)

---

Thank you. I will take a read today.