zlacker

>>datafl+(OP)
We don't want to know. That may sound a bit glib but I think it's true. What would be the reaction if we could determine the outbreak was due to an unintentional leak? China cannot reimburse the world for the economic damage covid has caused. It cannot be held accountable for all the lives that have been lost. It cannot compensate the world for the diminished quality of life we've all suffered. But there will be plenty of calls for China to do all of that. If covid is the result of Chinese negligence, the reaction and conflict across the planet over what to do about it is going to be absolutely terrible.

And let's not even begin to think what will happen if there were to be evidence that this was an intentional release.

>>Mounta+Ud
The China aspect is probably a red herring. Gain-of-function research was internationally funded, including by the US. The perils had been pointed out for years by virologists [1], some of whom managed to get an editorial in the New York Times against it [2].

If Covid turns out to be a lab escape (which is a big if), the nation or lab it happened in is just the proximate cause. Deeper responsibility would lie with the institutions and individuals that pushed it despite the risks. No one knows the answer to this (edit: I mean to whether covid escaped from a lab), but it's an open question that deserves credible investigation. Having the investigator be one of the principal funders of the research being investigated is such...bad optics, to put it nicely, that one wonders how anyone thought that would be ok.

[1] https://mbio.asm.org/content/3/5/e00360-12

[2] https://www.nytimes.com/2012/01/08/opinion/sunday/an-enginee...

>>guesst+vf
> If Covid turns out to be a lab escape (which is a big if),

It seems like we don't have evidence, but the natural evolutionary experiment that's occurred provides a staggering amount. We can see from the virus phylogeny that:

1. The virus entered the human population in October 2019. All known SARS2 sequences are related in a single clade that, under very soft assumptions about mutation rate, would coalesce in late fall 2019. The first sequences we got, in early 2020, had only a handful of mutations between them. Nothing has ever arisen outside of this clade.

2. The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein. We can see this because there was not an accelerated evolution in this protein. We did not see changes in the viral genome resulting in a significant phenotypic change until the b.1.1.7 and other "third wave" variants arose. This stands in intense contrast to every other zoonotic transfer we know of. Adaptation always occurs because biology is different enough that different viral configurations provide immediate gain, and through continuous mutation the virus is exploring a huge space of these all the time. The fact that it doesn't mutate rapidly indicates it is near a strong local optimum.

One way of understanding the significance of this is by thinking of the virus as a learned model which is learning a solution to the problem of its own survival. What this evidence shows is that is appeared already optimized. We see this because over an incredible number of update steps (many quadrillions perhaps, with each human infection being like a minibatch, and each viral replication like a step) there was no significant reduction in test loss (viral survival). We randomly picked a perfect initial model. Either that first virus was lucky in a way that is similar to guessing a perfect solution, which has a probability so low as to be fanciful, or it had already in incorporated all the readily-usa le information about the human ACE receptor.

Do we have evidence? What is the probability of this pattern occuring in the case of a natural spillover? It's 1:atoms-in-the universe level. Finding a virus already so optimized to humans by randomly sampling from existing ones is like the kind of collision probability level that we comfortably use to build cryptocurrency castles that assume key non-collision. In the case of a virus optimized by serial passage in the lab? Frankly it's indistinguishable from that.

>>inciam+nn
This is complete speculative junk.

> The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein.

1. Is a partially functional (still infectious) spike receptor protein possible? (you don't know, and present no evidence in this rant)

2. How do you know the virus shows "no accelerated evolution"...partially effective viruses would have a lower replication factor, and not become global pandemic, and would not spread far enough to preserved within the human population as anything of interest.

3. How do you know that a natural virus which was only partially effective at replication didn't in fact encounter favorable conditions when it encountered humans, having accidentally been better adapted for them?

> The fact that it doesn't mutate rapidly indicates it is near a strong local optimum.

4. How do you know that the spike protein - which is highly conserved amongst coronaviruses - can even have a range of mutations and still retain function (allowing viral entry to the cell for infectious purposes)? (you don't, research finds that the spike protein has suboptimal binding to ACE receptors - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239051/)

> This stands in intense contrast to every other zoonotic transfer we know of.

5. Does it? Because no research is proposing this. Research in fact finds that analysis of similar coronaviruses shows that the spike protein is likely the result of multiple recombinations between a few species (https://academic.oup.com/emph/article/2020/1/290/5956769).

> Do we have evidence? What is the probability of this pattern occuring in the case of a natural spillover?

6. Do you? Apparently not because there's not a single shred of peer reviewed research you care to link to support your position here, and you've done none of the legwork to support the logic part of your conclusions.