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Covid Mutations



That is a good video, but neither Racaniello or Drosten say that it isn't anything to worry about. Just that it needs further information and they don't agree with hyped up claims about it on the basis of evidence presented so far. Racaniello says in the video that an existing Singaporean mutation may be linked with less severe disease. He also says that he's not convinced of the methodology used to say that the virus is more transmissible, not that it's definitely not an issue.
 
I'm sure it's been covered elsewhere, but these ACE mechanisms in cells are presumably there for a reason ... what's the possibility that the natural or synthetic immunity to these spike proteins - even if not excatly like the ones found in the body will eventually cause long-term problems ?
 
I'm sure it's been covered elsewhere, but these ACE mechanisms in cells are presumably there for a reason ... what's the possibility that the natural or synthetic immunity to these spike proteins - even if not excatly like the ones found in the body will eventually cause long-term problems ?
What do you mean?
 
What do you mean?
My understanding of such things is very sketchy, but these viral spike proteins are close enough to being an exact "key" to gain entry to cells, and presumably the "lock" is there for legitimate body processes - though clearly not intended to let random strings of RNA in (though then we add the complication that we might need this for gene therapy - of which the vaccines are presumably a sort of crude version of) ...
So might it become problematic if we train our immune systems to leap on things that are a close emulation of the protein "key" ?
 
Surely that's the same with any virus or vaccine though?
So eventually something will show up that will mess up an important physiological process permanently ?
I suppose since we're using actual viral RNA code, we are at least matching the virus's own slightly inaccurate key ...

EDIT :- yikes ...
 
This is a feature of xRNA platform vaccines - rapid re-engineering. Need to add additional time for discovery, characterisation and regulatory approval, hence the ~2 months upthread.
 
That's not where I'm coming from - just trying to be as informed as I need to be without going back to college ...

You're throwing random bits of uneducated ideas around with no understanding of the science. You could start a new thread for that if it floats your boat.
 
You're throwing random bits of uneducated ideas around with no understanding of the science. You could start a new thread for that if it floats your boat.
Really ?
So no admission for non- graduates ?
Welcome to a very small echo chamber.
And success - I'm off to learn elsewhere.
 
Really ?
So no admission for non- graduates ?
Welcome to a very small echo chamber.
And success - I'm off to learn elsewhere.

Find something on your idea and bring it back here. As a user of ace2 inhibitors I'd be interested to find out more.
 

You'll need to use Google translate but this is interesting
Google Translate said:
Update from December 22nd

After initially confident statements, the virologist Christian Drosten is now concerned about the coronavirus mutation in Great Britain in the face of new data.
Try the previous page of this thread ;)
 
He seems to say it's concerning but mainly because of the level of infection itself?
That is correct. That is the main concern based on the results we have right now. That alone hikes up R which, aside from more immediate implications for mitigations, in turn has ramifications for vaccine uptake (will ultimately need to immunise a greater swathe of the population). Obviously also increases the number of cases per unit time which in turn will feed into widening the zoo of variants in a given timeframe; the more bioreactors*time you have the more likely you hit the 'interesting' variants sooner.
 
So the more people are infected the more variants can arise? If I understand Racaniello correctly, he said that everyone infected with covid had lots of viruses with different mutations in their lungs as the viruses also mutate between cells, he talked about the 'founder effect' where if someone coughed on someone then the viruses of a particular variant would establish themselves if they are the one who infected the person, and the viruses that arose would be derived from those mutations? Or have I got it totally wrong?
 
The more people there are infected, the longer they are infected, the more virions there are, and so, the more mutations, more variations will be seen. Eventually some of those will be selected (advantageous).
 
So the more people are infected the more variants can arise? If I understand Racaniello correctly, he said that everyone infected with covid had lots of viruses with different mutations in their lungs as the viruses also mutate between cells, he talked about the 'founder effect' where if someone coughed on someone then the viruses of a particular variant would establish themselves if they are the one who infected the person, and the viruses that arose would be derived from those mutations? Or have I got it totally wrong?

That’s basically right, although the mutation rate of this virus is pretty low, so for most people who have it the mix of varieties they start with isn’t likely to change all that much.

The founder effect is important though, and is where the selection pressure for better transmission comes from basically - when you’re coughed upon by an infected person, you’re enveloped in a cloud of all their virus varieties (assuming for the moment that all their varieties are as good at expressing in the airways and hence getting expelled) - the varieties that are better at transmission (whether by better binding to your cells, or better evasion of first-line immune defences) are more likely to make it into you - ie the less good at transmission ones get left behind. Your population of viruses is then on average better than the population in the previous person. You multiply them up and then cough on someone else and the ratchet happens again.

This doesn’t really happen every time of course, there’s a lot of randomness in it, plus confounding effects, such as for instance ability to multiply in your body: it might be that one of the not as good at transmission varieties is however much better at replicating when it gets inside you - so it might make up just 1% of your initiial infection, but by the time you’re ill enough to cough on other people it makes up 99% of your population, giving it a better chance of transmission just through numbers.

But on the whole that’s what it’s all about in this context.

Disclaimer: evolutionary biology and virology knowledge a good couple of decades rusty, but hopefully largely still fit for purpose.
 
Another way that transmission could be increased by a mutation (although am not saying this is the case with this one, I don't have enough info and it doesn't seem to be the case) would be if the infection made people sneeze more than other strains - that sprays a large area at a time. I don't think that is necessarily the case with this one though, if it still has a higher transmission rate even when people aren't exhibiting symptoms.
 
Another way that transmission could be increased by a mutation (although am not saying this is the case with this one, I don't have enough info and it doesn't seem to be the case) would be if the infection made people sneeze more than other strains - that sprays a large area at a time. I don't think that is necessarily the case with this one though, if it still has a higher transmission rate even when people aren't exhibiting symptoms.

There is some work on this summarised in this thread. I must say the differences don't look significant to me but I'm not a statistician.

 
A fairly comprehensive and accessible summary of where we are up to right now with the B.1.1.7 (VUI-202012/01) and related N501Y variants which brings together a lot of the material covered here and in adjacent threads the last few days.
 
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