The attachment protein “spike” of the new coronavirus SARS-CoV-2 uses the same cellular attachment factor (ACE2) as SARS-CoV and uses the cellular protease TMPRSS2 for its activation. Existing, clinically approved drugs directed against TMPRSS2 inhibit SARS-CoV-2 infection of lung cells.
ILLUSTRATION: MARKUS HOFFMANN
excess weight causes extra pressure on the heart and lungs. This will in fact put you in a higher risk group. I do agree that we need to open up but not because I dont think this thing is serious. I think unfortunately we did this half ass long term lock down instead of a 2 to 4 week real one.So now I am afraid it will become endimic if its not already. Maybe this virus is not as bad for all as we thought it was but it is still pretty bad. The argument keeps changing based on politics instead of facts. The bottom line is we are in worse shape than we were when the shelter orders came in. I say this because there is still no vaccine and way more cases here now than there was. Speaking of vaccines I would not hold my breath for one . They still havent found one for most of these viruses. What was the last vaccine made and how long did it take to get it? This is kind of a ramble but it worries me that the “healthy” and as far as I know includes me are going to just act like we are open now so back to business as usual Except that instead of starting with just a few cases we have tons.
Agreed about ACE2, but the text does just say drugs “inhibit” the infection of lung cells - so that’s quite relative, i.e. how much do they really do that? It’s not like any such drugs are broadly effective or in use, from what I can see. It’s the “German Primate Center” - they may just be talking about lung cells cultured in a dish. That website specifies that for both SARS and the new coronavirus, “No vaccines or drugs are currently available to combat these viruses.”
The diagram doesn’t address the difference between SARS and the Covid-19 causing virus, which is, as far as I know, rooted in the spike proteins. It’s not shown on the diagram, but SARS-CoV-2 has a physically different spike - it attaches to human receptors in a smaller, more compact way, It’s a stronger attachment, and this allows more efficient infection of human cells - this is why the new SARS spreads faster than the old one.
I see it as both SARS-Cov and SARS-Cov-2 insert their S protein key into the ACE-2 receptor lock. Anti-A antibodies latch onto the S protein key so the virus is unable to insert it into the ACE-2 receptor lock and therefore immune system cells can engulf the virus.
If the supposedly new S protein key fits differently into the exact same ACE-2 lock… would Anti-A antibodies which mimic ACE-2 receptors really not be able to latch onto the S protein?
I’ve noticed all my family members who are blood type O have very little symptoms while I felt like I was going to die. What other explanation is there?
About a billion possibilities, given it’s the human body. Correlation does not imply causation, and so on.
Many other explanations.
It’s a question - does it happen in this case, does it matter, etc?
I’m very open to hearing what these other or additional possibilities are.
What I’ve written is logical and self evident. Can viruses be engulfed without antibodies?
Let’s hear these other explanations. I’m always open to learning something new.
It does happen and it does matter because it’s a matter of fact.
I’d like to remind both of you that we’re talking about science. Not statistics. Therefore please don’t treat science as a statistic.
Okay, that’s cool. But all I see thus far is you guessing that a thing happens - that anti-A antibodies affect things. It was a thing with the first SARS, but is there any scientific proof that it operates with SARS 2?
We do know that SARS 2 is different. The first SARS essentially just died out on its own. Doesn’t look like that’s the case this time around. The spike proteins on SARS 2 are 10 to 20 times more likely to attach to human cells - this makes for the observed higher transmission rate and longer survival of the virus. The SARS 2 spike protein is 89% genetically similar to the first SARS. Pretty close but enough different to account for what we’re seeing.
Despite similarities in sequence and structure between the spikes of the two viruses, three different antibodies against the 2002 SARS virus could not successfully bind to the SARS-CoV-2 spike protein. This suggests that potential vaccine and antibody-based treatment strategies will need to be unique to the new virus.
That does not prove that what you assume cannot be true. But until there is some scientific proof that it does operate, we’re left with