Other methods exist, but we ran a meta-analysis that would've picked up these other methods, and those other methods were not commonly used in this field.
8/10 of the infectious clones we found retained these modified type II sites.
4/
Recombination is common in CoVs, but recombination can explain anything.
I could find green fluorescent mice in Bergen, Norway, and say it must be from recombination with a jellyfish.
That doesn't mean recombination is the most likely scenario. Further research is needed.
5/
The existence of these type II sites in other CoVs is proposed as evidence of recombination...
But that's also consistent with reverse genetic systems used to make chimeric viruses in the lab:
they require the same type II sites in the same place in order to swap parts.
6/
The recombination hypothesis is just that: a hypothesis
The researchers proposing recombination need to quantify odds & uncertainty of their hypothesis as we've done with our theory.
All other CoVs were subject to recombination, yet SARS-CoV-2 is an anomaly among CoVs.
7/
That's worth repeating:
Recombination happened in all other CoVs, and it never once in the CoVs we examined produced such an idealized reverse genetic system
We estimate under 0.07% chance of finding this in pattern nature
What are the odds, P-values etc. of recombination?
8/
Crucially, the sequences proposed as being behind the recombination events all appear to have issues being debated in the peer-reviewed literature.
We're uncertain these sequences are correct, so we're uncertain about recombination.
SARS-CoV-2 acquired the first-ever Furin cleavage site in a sarbecorivurs through *another* recombination event, acquiring two CGG codons uncommon in CoVs
This virus then caused an outbreak in Wuhan, incidentally a global hotspot of CoV research...
2/
Coincidentally,
The CoV research in Wuhan also included a grant proposal to create chimeric CoVs using the reverse genetic system that is makes SARS2 so anomalous
They also proposed to insert a Furin cleavage site into a sarbvecovirus.
3/
Here's @Telegraph quoting Stuart Neil falsely accusing us of cherry-picking, Kristian Andersen tactfully calling it "b*******", and someone going after credentials by saying I'm a "business management efficiency analyst"?
That same idea - the very strictly correct idea for the term "golden gate assembly" - led another smart scientist to think that, for our theory to be true, the BsaI/BsmBI recognition sequences must be in opposite orientation.
I'm unable to comment on this thread (having been blocked by Rasmussen) but it does seem like folk may be claiming to @KelseyTuoc that our work is fraud/deception/misconduct.
The multiple comparisons problem arises when you run many tests, describe the P-values or odds of seeing as-big-or-bigger a discrepancy under the null model, and fail to account for the fact that you ran many tests.
In our paper, we do evaluate the likelihood of many events under a null model - maximum fragment lengths, ideal no fragments, silent mutations, etc. - so it's fair to discuss multiple comparisons, what corrections we may want to make, and how we justify them.
3/