For you know if the ACE2 genes mentioned with relation to coronavirus have anything to do with ACE inhibitors and ARB inhibitors?
>The largest Chinese study with 44,672 confirmed cases of Covid-19 shows a high overall case fatality rate (CFR) of 2.3% [2]. Important co-morbidities are hypertension (CFR 6.0%), diabetes (CFR 7.3%), cardiovascular disease (CFR 10.5%) and age >70 (CFR 10.2%) [2]. Similar co-morbidities were noted for the SARS outbreak in 2003.
> ...
>On the one hand, it has been shown that the Covid-19 agent (also known as SARS-CoV-2), uses the SARS-COV receptor angiotensin converting enzyme (ACE) 2 for entry into target cells [4]. The interface between ACE2 and the viral spike protein SARS-S has been elucidated and the efficiency of ACE2 usage was found to be a key determinant of SARS-CoV transmissibility [4].
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>On the other hand, it could be shown in animal experiments that both the ACE-inhibitor lisinopril and the angiotensin-receptor blocker losartan can significantly increase mRNA expression of cardiac ACE2 (5-fold and 3-fold, respectively) [5]. Further, losartan also significantly increases cardiac ACE2 activity [5].
Edit: thank you philipn for your twitter link.
https://twitter.com/__philipn__/status/1235756671852589056
It may be the other way around: ACEi/ARB may be protective. HTN without ACEi/ARB would be non-protective, potentially so much so that it skews the group fatality numbers. This is because people with HTN have a different renin-angiotensin system profile: more AT1R, less AT2R, more ACE, potentially less ACE2.
This is being looked at now. But the key is that in every study ever done on viral lung disease, etc, AT1R blockade was highly beneficial, and we know that ACE2-knockout basically screws up lungs, makes viral lung disease way worse, etc. Please see my twitter posts.
The virus eats up ACE2, downregulating it as it binds. This would have delirious effects. Check out the linked "essential reading" twitter post.
Will be posting a summary to my twitter soon.
It's only the scientists who didn't start studying Coronaviruses until two weeks ago who seem to think that having ACE2 receptors is dangerous.
Which country are you in?
Edit: Luckily I own several acres of Hawthorn bushes.
I'm not 100% sure on the mechanism of action on Hawthorn. I've read that it's an ACE inhibitor, but I don't have a good source. But I can see at the very least that it's an elastase inhibitor, which is supposed to be protective against ARDS.
edit: I think proanthocyanidin is the component that is supposed to be an ACE inhibitor.
Sources:
https://www.ncbi.nlm.nih.gov/pubmed/12866623
https://www.phcogj.com/sites/default/files/PharmacognJ-10-25...
Do you take them like some herbal remedies (grind it, add honey etc.etc) or do you process it in a lab?
People make their own hawthorn jam and jelly though, so it isn't excessively dangerous, but on principle it's probably better to take a conservative approach, or at least one that's commensurate with the initial risk.
Because I'm in NYC we actually have them growing everywhere because they are one of a handful of approved small-sized street trees, and they're in all the parks, but regardless it's easier just to buy as a supplement.
I'm taking a low dose though, in part to hedge my bets, and in part because I don't want to bleed out if I get into a bike accident.
As per the paper, you want to either block the receptor or down regulate it.
There are also many other ways you can block the virus from entering your lungs that don't involve downregulating your ACE2 receptors.
https://www.nejm.org/doi/full/10.1056/NEJMoa2002032
86.9% of non severe cases had never smoked 77.9% of severe cases had never smoked
Contrasted with 1.3% and 5.2% in former smokers and 11.8% and 16.9% in current smokers.
For instance, there are 137 current smokers. 108 are listed as non-severe. 29 are listed as severe. This means 108/137 = 79% non-severe, 29/137 21% severe.
Never smoked: 927 total, 793/927 non-severe (86%), 134/927 severe (14%).
Hope that makes sense. That table confused me too. Don't start smoking!
When this came up for discussion on HN a few days ago, I was initially confused, as some of what I read seemed to suggest that taking e.g. lisinopril could possibly increase the risk of an infection because it seems to increase the expression of ACE2 receptors that are used by the virus to infect cells.
On the other hand, some of what I read seemed to suggest that ACE inhibitors (e.g. lisinopril) could have a therapeutic benefit. The virus is going to inactivate a bunch of ACE2 receptors through the course of infection. Since ACE2 receptors inactivate angiotensin, that would leave a lot of active angiotensin floating around, which is potentially very bad. ACE inhibitors would seem to help here because they inhibit the active form of angiotensin from being created in the first place.
Now I'm wondering: Is it possible that taking lisinopril could increase the risk of serious infection for those of us not yet infected, but also could reduce the severity of an active infection?
Elderly people are usually on BP meds. Diabetics are frequently prescribed Losartan to protect their kidneys. I know. I am a diabetic, and was prescribed it for that reason and also for high BP.
As a diabetic over 50 with high BP I have a greater interest than most. Especially since my wife was exposed to coronavirus, is sick, and I am starting to feel unwell.
Stopped taking losartan yesterday. Have some tenofovir lying around and might start taking it. It's the only antiviral I was able to get my hands on. Hopefully my chloroquine arrives in the mail soon.
https://www.dpz.eu/en/home/single-view/news/die-vermehrung-v...
1. lungs are highly vascularised areas with a large amount of vascular endothelium, making them a great location to express ACE if you want to convert as much angiotensin I as you can in the space of a heartbeat (which you'd like to do if your blood pressure dropped, for example).
2. ACE is not specific for angiotensin, it acts on a variety of peptides. Bradykinin is a good example as it can provide more perspective on why ACE is expressed mainly in lung tissue. Bradykinin acts to contract smooth muscle in your airways. Thus, degrading bradykinin via ACE is a good way to improve your breathing.