Since none of the closest wild relatives carries a furin cleavage site while sharing nearly everything else, the FCS is a discriminating feature whose acquisition is a separate event not explained by these bat genomes, leaving its route to be determined.
Reasoning
The BANAL viruses match SARS-CoV-2 closely across the genome and at the ACE2 interface, yet uniformly lack the polybasic furin cleavage site at S1/S2. Therefore the wild-relative pool can account for the backbone and the human-ACE2-binding RBD but not the FCS. Logically the FCS must have been gained after SARS-CoV-2’s lineage diverged from these bats, as an independent event. This sharpens rather than resolves the origins question: the closest natural genomes remove the RBD from the list of features requiring special explanation but leave the FCS’s mode of acquisition (recombination with an as-yet-unsampled virus, in-host insertion, or otherwise) open.
Validity verdict — approved (checked)
Reconstruction. Premise: the BANAL viruses match SARS-CoV-2 closely across the genome and at the ACE2 interface yet uniformly lack the polybasic FCS. Load-bearing step: from “closest relatives lack the FCS while sharing nearly everything else” to “the FCS is unaccounted for by these genomes and so was acquired as a separate event, route undetermined.”
Evaluation. Near-deductive and holds conditional on the premise: if the closest sampled relatives lack the feature, those genomes cannot supply it, so its acquisition is a distinct event in the lineage. Probed defeater: “the FCS could be ancestral and lost in the BANAL lineages rather than gained in SARS-CoV-2.” This does not defeat the stated, deliberately modest conclusion — under a loss scenario these particular genomes still fail to explain the FCS and its route still remains to be determined, which is all the argument asserts (it stops short of claiming natural vs lab). No defeater survives against the conclusion as stated. Traced here → checked.