COVID origins — The FIPV is not the lynchpin of case for the lab leak hypothesis, it is the cherry on top. The main arguments for the lab leak case rest on the location and timing of the SARS2 outbreak coinciding with WIV coauthoring the DEFUSE proposal and setting out to look for novel SARS-like CoVs that are 10-25% different in their spikes from SARS1.
Then there is the presence of the FCS in SARS2 so uncharacteristic of SARS-like CoVs, especially in light of DEFUSE proposing to engineer novel FCSes in SARS-like CoVs.
And then there is the AUTHOR of this idea — Ralph Baric himself — explaining WHY he proposed to do this in DEFUSE and citing FIPV as the inspiration behind his idea — set against the backdrop of three lethal strains of FIPV containing the very same PRRAR FCS as SARS2, which btw includes the leading proline, just like MERS, another favorite virus of WIV, Ralph Baric, Fang Li etc.
So in my book it’s very plausible that whoever decided to take Baric‘s DEFUSE idea of engineering novel FCSes in SARS-like CoVs and run with it decided to also use the most frequent FCS in lethal FIPV strains as one of the candidates for (likely several) new FCSes to try engineering into SARS-like CoVs — as FIPV was an inspiration to try doing so in the first place.
While I agree that ENaC FCS is a red herring (what relevance does a specific FCS motif in a subunit of some human Na channel have to coronaviruses??), I wouldn’t dismiss the FIPV connection — as Baric said, the observation that when FIPV’s FCSes mutate to become less cleavable this turns the virus from benign to lethal was *the* inspiration behind proposing to engineer novel FCSes in SARS-like CoVs in DEFUSE, and three known lethal strains of FIPV have the same PRRAR FCS as SARS2. And their nucleotides match save for the codon choice for the arginine doublet — AGA vs. CGG: