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1. thowaw+(OP)[view] [source] 2021-05-24 00:56:59
There are numerous reasons why we need a proper investigation into this. If this came out of WIV, we need to determine exactly why these bat coronaviruses were being studied with regards to human ACE2.

This ACE2 binding is causing numerous issues, including damage to human heart, lung, kidney, and pancreatic cell death.

This is serious stuff. If anyone is looking at the "low" mortality rate, they are missing the big picture.

Role of angiotensin-converting enzyme 2 (ACE2) in COVID-19

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7356137/

The genetic structure of SARS‐CoV‐2 does not rule out a laboratory origin

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7744920/

SARS-CoV-2 infects human pancreatic β-cells and elicits β-cell impairment

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)...

replies(4): >>Dah00n+23 >>lamont+Om >>koheri+Gp1 >>giardi+wP1
2. Dah00n+23[view] [source] 2021-05-24 01:28:29
>>thowaw+(OP)
>we need to determine exactly why these bat coronaviruses were being studied

Why do we need evidence of why a lab would do research in viruses that is a danger to people in the country? It's pretty self-explanatory. ACE2 isn't specific to SARS-CoV-2 as your own links says.

3. lamont+Om[view] [source] 2021-05-24 06:16:18
>>thowaw+(OP)
HCoV-NL63 enters cells via ACE2 and only causes the common cold.
replies(1): >>thowaw+gw
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4. thowaw+gw[view] [source] [discussion] 2021-05-24 08:16:22
>>lamont+Om
Very interesting. This is certainly a scientifically valid response.

> Here we show that SARS-CoV, but not HCoV-NL63, utilizes the enzymatic activity of the cysteine protease cathepsin L to infect ACE2-expressing cells.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142358/

replies(1): >>lamont+HE1
5. koheri+Gp1[view] [source] 2021-05-24 15:31:59
>>thowaw+(OP)
ACE2 binding is common among coronaviruses. This is neither unique to covid-19, nor uncommon generally.
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6. lamont+HE1[view] [source] [discussion] 2021-05-24 16:37:24
>>thowaw+gw
The vastly more likely significant differences are:

1. We don't (yet) inherit antibodies to SARS-CoV-2 from our mothers.

2. SARS-CoV-2 has not been forced to make evolutionary sacrifices to evolve to escape immunity.

The virus has the freedom to become optimally bad and our immune systems were optimally naive.

Over time the warfare between our immune system and the virus should cause SARS-CoV-2 to look a lot more like HCoV-NL63.

That's a sufficient explanation of the differences in disease severity without having to troll through medical articles.

7. giardi+wP1[view] [source] 2021-05-24 17:23:26
>>thowaw+(OP)
thowaway959125 says> "it would be great if we took this opportunity to actually end biological weapons research globally."

The genii is out of the bottle so ending biological weapons research will never happen. If we aren't hit by a nation-state using biological warfare then we'll be hit by someone who does biochem in his garage for fun.

The best strategy is to advance the research while taking such steps as creating super-vaccines to make this type of biowarfare obsolete:

https://weather.com/en-IN/india/coronavirus/news/2021-04-21-...

But that also moves us one step closer to the "grey goo" scenario:

https://en.wikipedia.org/wiki/Gray_goo

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