COVID-19: Medical and Scientific Information

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NationalTitles18

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A question going through my mind:

What role are ACE2 serum antibodies thought to have in relation to COVID-19 manifestations? If those infected are producing these antibodies in response to infection, or perhaps already have them prior to infection, could this explain COVID toes (digital ischemia and vasculopathy), hypercoagulation, endothelial injury and some other manifestations of the disease?

The first link:
Quote: Angiotensin-converting enzyme (ACE) 2, a homolog of ACE, converts angiotensin (Ang) II into Ang(1-7), and the vasoprotective effects of Ang(1-7) have been documented. We explored the hypothesis that serum autoantibodies to ACE2 predispose patients with connective tissue diseases to constrictive vasculopathy, pulmonary arterial hypertension (PAH), or persistent digital ischemia.

https://arthritis-research.biomedcentral.com/.../ar3012

The second link:
Quote: The aim of the present study was to test the hypothesis that the activation of the angiotensin-converting enzyme (ACE)2/angiotensin-(1-7)/Mas receptor axis by use of a novel ACE2 activator (XNT) would protect against thrombosis....Thus, a decrease in thrombus ACE2 activity is associated with increased thrombus formation in SHR. Furthermore, ACE2 activation attenuates thrombus formation and reduces platelet attachment to vessels.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811560/
 

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Important - "re-positive" patients found not to be infectious...

Bloomberg
I was just going to post that....this is huge for the effectiveness of a vaccine.

Also for the development of better tests. Since the existing test can't tell the difference between a live virus and fragments of dead ones, it effectively generates a lot of false positives -- not good for anybody.
 
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TIDE-HSV

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I was just going to post that....this is huge for the effectiveness of a vaccine.

Also for the development of better tests. Since the existing test can't tell the difference between a live virus and fragments of dead ones, it effectively generates a lot of false positives -- not good for anybody.
It also explains some of the "false" negatives. We know so little about the disease, it's possible that the body's process of clearing the remnants of the virus are intermittent, in bursts, depending on functions we are as yet unaware...
 
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NationalTitles18

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NationalTitles18

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May be bias involved
Precisely why I stayed silent on it, although there is a basis for the plausibility since several cannabinoids are known anti inflammatories and it's at least possible they could modulate the inflammatory "phase" of the disease. Mrs. NT17 got a good laugh the other day speculating cannabis as the cure and the pearl clutching back home. :D

ETA: The last bit was a social observation and not intended as a political statement.
 
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TIDE-HSV

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Precisely why I stayed silent on it, although there is a basis for the plausibility since several cannabinoids are known anti inflammatories and it's at least possible they could modulate the inflammatory "phase" of the disease. Mrs. NT17 got a good laugh the other day speculating cannabis as the cure and the pearl clutching back home. :D
I thought it was worth throwing out there FWIW, with the notation because it's being funded by pro-cannabis sources. Also, if it really reduces your ACE2 receptors by 70%, that's not without consequences. If it blocks the virus spikes' being able to attach to the receptors, then that's a different story...
 
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NationalTitles18

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I thought it was worth throwing out there FWIW, with the notation because it's being funded by pro-cannabis sources. Also, if it really reduces your ACE2 receptors by 70%, that's not without consequences. If it blocks the virus spikes' being able to attach to the receptors, then that's a different story...
Yep. Not criticizing the post. I was just waiting for more data. Hard to NOT get a biased source on cannabis research, especially in the US. (I know this was in Canada)
 
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