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Hey @Ikaika -- I read this today and wondered if you had seen this/had any thoughts.


I know it's not a scientific/medical journal, but I think it makes a lot of sense.

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this makes a lot sense since we know that the target for this virus are any cells that harbors the ACE-2 receptor. One such cells that contain this receptor, endothelial cells. Endothelial cells line the blood vessels and chambers of the heart. So, yea, this is not too surprising.
 

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this makes a lot sense since we know that the target for this virus are any cells that harbors the ACE-2 receptor. One such cells that contain this receptor, endothelial cells. Endothelial cells line the blood vessels and chambers of the heart. So, yea, this is not too surprising.
My thought was would ACE inhibitors help to slow the progress of the disease?

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My thought was would ACE inhibitors help to slow the progress of the disease?

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Unfortunately, the ACE inhibitor links onto a different domain than the virus to this receptor-enzyme. So, the ACE-inhibitor does not inhibit the S1 domain of the spikes of the coronavirus from linking onto the receptor, it only inhibits the angiotensin I.
 

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Unfortunately, the ACE inhibitor links onto a different domain than the virus to this receptor-enzyme. So, the ACE-inhibitor does not inhibit the S1 domain of the spikes of the coronavirus from linking onto the receptor, it only inhibits the angiotensin I.
I only understand about 50% of that, but I appreciate the response and your attempt to explain it to me.

I understood the most important part, "Nice thought, but it won't work." I trust that the rest is accurate, because you are a scientist and I am not.

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I only understand about 50% of that, but I appreciate the response and your attempt to explain it to me.

I understood the most important part, "Nice thought, but it won't work." I trust that the rest is accurate, because you are a scientist and I am not.

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Not necessarily the classic ACE-inhibitors, there are some medications related to ACE inhibitors that are being tested to combat this virus. So, your initial instinct was spot on.
 

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If any of you are a fan of audible and interested in the topic of infectious disease, I have a recommendation:

The Great Courses series

”An Introduction to Infectious Diseases” by Professor Barry C Fox
 

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A trial began today for a therapy(treatment of sick patients) using antibodies. Results on how safe it is are expected by month's end, but apparently they won't know how effective it is until a second phase of testing. It may also be useful for preventing the disease.
 

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There is some new preliminary evidence that SARS-CoV-2 in Europe may have gone through some major mutational events that is rendering this virus less contagious than it first presented itself as in Dec - March.

Nothing has been published on it yet, just noise in the science forums.
It seems counterintuitive to this lay person that a less contagious version would become more prevalent, but there's probably something I don't understand.
 

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It seems counterintuitive to this lay person that a less contagious version would become more prevalent, but there's probably something I don't understand.
You are referring to Lamarckism, a form of evolution that has long since been an unaccepted theory. This, opposed to the accepted theory of evolution that is based on random mutations that lead to iterations. The iterations that allow for survival of the fitter. Some mutations may lead to a more contagious other mutations, less... it does not mean that this mutational iteration will survive, it is just the one that has been isolated as of late.
 

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It seems counterintuitive to this lay person that a less contagious version would become more prevalent, but there's probably something I don't understand.
The only goal of a virus is to replicate. The fact that the host may get sick or die is just a side effect. But a virus which is has a lot of negative effects will have trouble surviving because either the host will die too quickly or the community will make changes to hinder people getting infected. The latter is what we saw with the CV19 virus. Whole communities shut down because people were dying and hospitals were overwhelmed, which meant the virus couldn't find hosts and replicate as easily. But if another strain of the virus that doesn't cause as many negative consequences becomes more prevalent, the shutdowns are relaxed, people congregate again, and the virus will have more hosts to infect. So the less contagious version could become more prevalent because society will open up more when that version is the dominant strain in that community.

It's important to realize that it's not a single strain of the virus that is becoming less contagious. Rather, it's that the virus mutates constantly and there new and different strains in the community. The strains which have an optimum rate of infection compared to the negative consequences will be most successful.
 

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You are referring to Lamarckism,
No, I'm not.
a form of evolution that has long since been an unaccepted theory. This, opposed to the accepted theory of evolution that is based on random mutations that lead to iterations. The iterations that allow for survival of the fitter. Some mutations may lead to a more contagious other mutations, less... it does not mean that this mutational iteration will survive, it is just the one that has been isolated as of late.
My understanding of evolution is based upon random mutations, but it seems like a more contagious version of the virus will be replicated more, leave more descendants and eventually replace the less contagious one.
 

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The only goal of a virus is to replicate.
Not sure they have any goals, but that is the major part of their survival.
The fact that the host may get sick or die is just a side effect.
Sure.
But a virus which is has a lot of negative effects will have trouble surviving because either the host will die too quickly or the community will make changes to hinder people getting infected. The latter is what we saw with the CV19 virus. Whole communities shut down because people were dying and hospitals were overwhelmed, which meant the virus couldn't find hosts and replicate as easily. But if another strain of the virus that doesn't cause as many negative consequences becomes more prevalent, the shutdowns are relaxed, people congregate again, and the virus will have more hosts to infect. So the less contagious version could become more prevalent because society will open up more when that version is the dominant strain in that community.

It's important to realize that it's not a single strain of the virus that is becoming less contagious.
Do we know this?
Rather, it's that the virus mutates constantly and there new and different strains in the community. The strains which have an optimum rate of infection compared to the negative consequences will be most successful.
If I understand the bolded part correctly, the different strains w/ difft. levels of contagiousness are all present in the same community, which means all will face the same mitigation efforts, or lack thereof, and other factors being the same, the more contagious ones will out-propagate and become more prevalent.
 

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No, I'm not.

My understanding of evolution is based upon random mutations, but it seems like a more contagious version of the virus will be replicated more, leave more descendants and eventually replace the less contagious one.
Not necessarily... if it is not fatal mutation, then it will survive. Remember this is just one of many iterations discovered recently. It does not mean that this is the only one or the only one that is dominant among all the vectors.
 

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Not necessarily... if it is not fatal mutation, then it will survive.
You're right, I should have said "eventually outnumber the less contagious one", not "replace the less contagious one".
Remember this is just one of many iterations discovered recently. It does not mean that this is the only one or the only one that is dominant among all the vectors.
I'm not disagreeing w/ any of this, it just seems being less contagious means it would become less prevalent over time and not more prevalent.
 

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You're right, I should have said "eventually outnumber the less contagious one", not "replace the less contagious one".
I'm not disagreeing w/ any of this, it just seems being less contagious means it would become less prevalent over time and not more prevalent.
Evolution does not follow a rhyme or reason... it is based on random mutations. And, while survival of the fitter follows these random mutations, it is not always easy to follow a direct path of what that means. So, less contagious but better fit to survival in the host may actually be the fitter adaptation.
 

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Some of the most severe symptoms may have more to do with our own immune system rather than the virus itself. That is our immune system is actually ridding the virus in a cytokine storm which results in some pretty severe and long-lasting symptoms. And, likely why some though Chloroquine would work, since it works with other autoimmune syndromes.

So a virus that is not going to be killed off so quickly but in doing so leaves less contagious may be the survival of the fitter. It is hard to know, I am merely speculating.
 

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Evolution does not follow a rhyme or reason... it is based on random mutations.
I think of the mutations as random, but differential survival as occurring for some reason, though not always a transparent one.
And, while survival of the fitter follows these random mutations, it is not always easy to follow a direct path of what that means. So, less contagious but better fit to survival in the host may actually be the fitter adaptation.
And if it turns out the less contagious ones happened to have better survival, they might well gain prevalence. But this is a possibility and not, so far, a likelihood and I was only talking about probabilities.
 
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