As far as I'm concerned it's largely irrelevant, because the real question is how the governments all handled the Covid crisis, once it was out in the open.
We need to know so we don’t do it again.
I’m not concerned about whether the car driver was drunk, I’m more concerned about how the paramedics responded to the crash.
In that sense, I hope that it was a lab leak. It will be better for us humans.
It wasn't uniquely adapted to humans in the beginning. Humans are just more connected species than for example panthers.
As it grew to pandemic levels it spawned mutations slightly more adapted to humans.
Seems wrong.
https://www.nature.com/articles/s41598-021-92388-5#Abs1
>Conspicuously, we found that the binding of the SARS-CoV-2 S protein was higher for human ACE2 than any other species we tested, with the ACE2 binding energy order, from highest to lowest, being human > pangolin > dog > monkey > hamster > ferret > cat > tiger > bat > civet > horse > cow > snake > mouse.
>>These findings show that the earliest known SARS-CoV-2 isolates were surprisingly well adapted to bind strongly to human ACE2, helping explain its efficient human to human respiratory transmission.
There's really no wonder that virus that spreads through human population is slightly better adjusted to humans than animal species its ancestor was infecting.
It's the case of water in the puddle surprised how well the puddle shape fits the water shape.
What I'm saying is that this virus is sufficiently general that it can infect multiple species with high efficiency and if hamsters were more densly connected than humans it could have been a hamster pandemic before it would become human pandemic.
This virus fits us well but not uniquely well.
This does not make sense to me, because I think the COVID virus was pretty stable for a long time (being an RNA virus and all that, I don't know). So the idea is that it was optimally adapted during the time of the jump to humans (of course it could have got the perfect mutation right at the time of the jump, but the chances of that happening is astronomically small), and the optimal human transmission was not acquired later when it started circulating in humans.
So the only way to have this happened is if it was optimized in a GoF research in a lab.
It easily infects species other than humans.
It's stable but not that stable. The variant that spread out of China was already different than the variant that initially caused trouble in China. Since then we got few new variants and that's only counting the ones that spread enough for us to notice.
There are no perfect things in biology. All things are just good enough. This virus was just good enough at spreading between people that given our connectivity it spread pandemically.
If the virus was was somehow uniquely well adapted to humans (which it isn't) it would be still more probable that its ancestor was just an unknown human coronavirus (other than 4 that cause some common colds) that we haven't discovered yet, because it spread completely asympthomatically. And the mutation it acquired made it slightly lethal not more infectious.
I don't think that happened because then why would pangolins be better suited for it than dogs, although dogs and cats being high on the list is quite curious.
And I'd be careful about reasoning that if I can't imagine any other way something could happen then it must have happened exactly the way I think it happened. It's good to be aware that no matter who I am and what I know, my ignorance always exceeds my knowledge and imagination.
To be frank, no one said so.
>And I'd be careful about reasoning that if I can't imagine any other way something could happen then it must have happened exactly the way I think it happened
No one is doing that either. Just that the chance of alternative is astronomically small..
There's nothing unexpected about Covid being infective because spread in humans is why we took note of it and are currently discussing it. That is, we're discussing P(human infectiousness | human epidemic). If we _randomly selected_ a virus from amongst _all_ viruses, then yes, P(human infectiousness) would be expected to be low, but we're not doing that. The former is plain selection bias (by which I mean the technical error; I'm not accusing you of bias).