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sarahbell

It's not the flu, it's just a very naughty virus

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Posted (edited)
41 minutes ago, sarahbell said:

the virus wreaks havoc wherever it can gain intracellular access

It gains access that via the cell surface ACE2 protein

Our cells with ACE2 that are exposed to the environment occur on the tongue epithelium that is highly enriched (no French kissing folks) and the alveoli of our lungs, so they are the 2 principal routes of entry from outside.

From the lungs it can gan access to our blood where the vessels are lined by endoltehial cells bearing ACE2 and then, via our circulation, to all other ACE2 bearing cells in our body, heart, kidneys, brain etc.

 

 

 

 

Edited by Hopeful

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2 minutes ago, Hopeful said:

the virus wreaks havoc wherever it can gain intracellular access

It gains access that via the cell surface ACE2 protein

Our cells with ACE2 that are exposed to the environment occur on the tongue epithelium that is highly enriched (no French kissing folks) and the alveoli of our lungs, so they are the 2 routes of entry from outside.

From the lungs it can gan access to our blood where the vessels are lined by endoltehial cells bearing ACE2 and then, via our circulation, to all other ACE2 bearing cells in our body, heart, kidneys, brain etc.

 

 

 

 

Is that a good thing or a bad thing?

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Any research that shows real learning, and shows that it can be potentially beaten without the "help" of Super Wavy Hands Nerd Nutter Boy, has to be welcomed.

I'm guessing the Gates tendrils have not reached this particular researchers lab yet.

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Posted (edited)
18 minutes ago, Wight Flight said:

What you said.

 

Firstly, SarsCov2 has much greater affinity for ACE2 than SarsCov, so it is much more infectious.

Binding of SarsCov2 to ACE2 downmodulates the ACE2 receptor, and in the lungs, this promotes tissue damage.
Elsewhere, its interaction with ACE2 (a crucual protein in the RAS system (The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance) has similar damaging effects.

MedCram on YouTube has covered this well. His explanations of the fundamental biochemistry are very good and I haven't seen any errors.

Edited by Hopeful

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7 minutes ago, Hopeful said:

 

Firstly, SarsCov2 has much greater affinity for ACE2 than SarsCov, so it is much more infectious.

Binding of SarsCov2 to ACE2 downmodulates the ACE2 receptor, and in the lungs, this promotes tissue damage.
Elsewhere, its interaction with ACE2 (a crucual protein in the RAS system (The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance) has similar damaging effects.

MedCram on YouTube has covered this well. His explanations of the fundamental biochemistry are very good and I haven't seen any errors.

So bad then?

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Posted (edited)
45 minutes ago, sarahbell said:

So why the variation in effects on individuals?

Did you really mean to ask that, or is it just early in the morning ? :) So many factors

No two individuals have the same genotype or ecophenotype. Here are just some examples

i) Everybody's immune system is slightly different,

ii) Everybody's abundance and distribution of ACE2  (the cell surface protein the virus interacts with) is slightly different - For example, adipose (fat) tissue expresses ACE2, not only are people of different weights but body fat distribution differs between sexes,

iii) ACE2 has a protective role in the lungs against acute respiratory distress syndrome (ARDS). ACE 2 levels are influenced by smoking (down regulates) and ACE inhibitor drugs (up regulates), diabetes (down regulates). The interaction between ACE2 and SarsCov2 is complex, however. Low levels of ACE2 may reduce the opportunity for infection (hydroxychloroquine may work by changing the glycosylation of ACE2 so that SarsCov2 can no longer bind to it to gain cellular entry), but once SarsCov2 binds with ACE2, ACE2 is effectively down-modulated and, post infection, ACE2 may be necessary for a good response - so a rock and a hard place.

iv) An individual's immune response is influenced by their Vitamin D level, which is influenced by diet, sun exposure, obesity, diabetes, age,

v) Different people have differing blood clotting responses, physiologies due to genotypic differences,

vi) People's diets differ, which not only influences their immune system but also intracellular and blood-levels of oxy-radicals that interact with the RAS system, of which ACE2 is a key component,

vi) So, people are very different as a result of genotype and evnironment, which is good. Just think if they were all like me.

As far as I understand it, the key variables that we can influence are our Vit D levels, diet and obesity. We can also perhaps influence our ACE2 levels via nicotine, but the interaction between the virus and ACE2 is so complex it's a difficult one to judge ATM IMO.

So I'm sticking with Vit D, diet and weight.

 

Edited by Hopeful

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19 minutes ago, sarahbell said:

So why the variation in effects on individuals?

seems to be something to do with genetics for some, there was something on the radio about it targeting dementia patients in care homes and it turned out to be a gene they had.

Even though it seems less dangerous I'm still wary of catching it due to the long term effects, though may have already had a mild version of it. 

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2 hours ago, Hopeful said:

Did you really mean to ask that, or is it just early in the morning ? :) So many factors

So I'm sticking with Vit D, diet and weight.

 


I did mean to ask that.

For a disease to be able to be asymptomatic in some people to having death as a major option is pretty wide ranging.

 

 

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2 minutes ago, sarahbell said:


I did mean to ask that.

For a disease to be able to be asymptomatic in some people to having death as a major option is pretty wide ranging.

 

 

 

1*IZ2II2HYKeoMrdLU5jW6Dw.png

 

https://towardsdatascience.com/understanding-the-68-95-99-7-rule-for-a-normal-distribution-b7b7cbf760c2

 

The question is how much have we skewed the distribution by creating and  enabling ill-health.

 

skewed-left.png

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3 minutes ago, Hopeful said:

 

1*IZ2II2HYKeoMrdLU5jW6Dw.png

 

https://towardsdatascience.com/understanding-the-68-95-99-7-rule-for-a-normal-distribution-b7b7cbf760c2

 

The question is how much have we skewed the distribution by creating and  enabling ill-health.

 

skewed-left.png

And Vitamin D presumably has a distribution chart too.

Anyone who has spent the last 10 weeks cowering inside is now presumably more at risk than they would have been if they've been having an hours compulsory sunbathing every day

 

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22 minutes ago, sarahbell said:


I did mean to ask that.

For a disease to be able to be asymptomatic in some people to having death as a major option is pretty wide ranging.

 

 

I said a while back this thing almost seems like an allergic reaction to the small amount of people who get very ill or die with it. 

This is based on zero expertise but I don't care I shall stick with it :D

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