Unsurprising, mutation is the hallmark of the corona viruses in the wild.
I read elsewhere that for genetically engineer viruses (which there is speculation that this may be the case here) are quick to lose their alterations via the natural mutation process.
In any case, more contagious doesn't mean more deadly, and that's probably what's most important.
> I read elsewhere that for genetically engineer viruses (which there is speculation that this may be the case here) are quick to lose their alterations via the natural mutation process.
It's speculated that the genetic engineering in this case was for “gain-of-function”, specifically to enable it to infect humans, so it's unlikely to lose its alteration.
The fact that the deeper you dive into the research activities of coronavirologists over the past 15–20 years, the more you realize that creating chimeras like CoV2 was commonplace in their labs. And CoV2 is an obvious chimera (though not nesessarily a lab-made one), which is based on the ancestral bat strain RaTG13, in which the receptor binding motif (RBM) in its spike protein is replaced by the RBM from a pangolin strain, and in addition, a small but very special stretch of 4 amino acids is inserted, which creates a furin cleavage site that, as virologists have previously established, significantly expands the “repertoire” of the virus in terms of whose cells it can penetrate.
> In any case, more contagious doesn't mean more deadly, and that's probably what's most important.
It does mean that because there is more than one strain out there, you may be immune to one but not the other, and that it seems to be more likely that it will continue to mutate and reinfect again and again, just like the common cold or flu. How many courses of this disease can you take, considering each one leads to what seems to be permanent lung damage?
3 comments
[ 2.4 ms ] story [ 30.4 ms ] threadI read elsewhere that for genetically engineer viruses (which there is speculation that this may be the case here) are quick to lose their alterations via the natural mutation process.
In any case, more contagious doesn't mean more deadly, and that's probably what's most important.
It's speculated that the genetic engineering in this case was for “gain-of-function”, specifically to enable it to infect humans, so it's unlikely to lose its alteration.
From https://medium.com/@yurideigin/lab-made-cov2-genealogy-throu...
The fact that the deeper you dive into the research activities of coronavirologists over the past 15–20 years, the more you realize that creating chimeras like CoV2 was commonplace in their labs. And CoV2 is an obvious chimera (though not nesessarily a lab-made one), which is based on the ancestral bat strain RaTG13, in which the receptor binding motif (RBM) in its spike protein is replaced by the RBM from a pangolin strain, and in addition, a small but very special stretch of 4 amino acids is inserted, which creates a furin cleavage site that, as virologists have previously established, significantly expands the “repertoire” of the virus in terms of whose cells it can penetrate.
> In any case, more contagious doesn't mean more deadly, and that's probably what's most important.
It does mean that because there is more than one strain out there, you may be immune to one but not the other, and that it seems to be more likely that it will continue to mutate and reinfect again and again, just like the common cold or flu. How many courses of this disease can you take, considering each one leads to what seems to be permanent lung damage?