Uses an explicit recombination-aware Bayesian phylogenetic framework (rather than a single fixed tree) to reconstruct the ancestry of the receptor-binding domain (RBD) across SARS-CoV-2 and its closest known bat/pangolin relatives (RaTG13, pangolin-CoVs, etc). Detects a recombination event on the branch leading to RaTG13, and infers that the RBD’s key ACE2-binding residues were most likely already present in the common ancestor of SARS-CoV-2 and RaTG13 — i.e. RaTG13 subsequently lost several of these residues via recombination with an unsampled lineage, rather than SARS-CoV-2 gaining them. Bears on the “did SARS-CoV-2’s key binding residues arise naturally in a wild ancestor, or look like an engineered/selected addition” question from the recombination-and-tree-topology side (as opposed to slice D’s sequence-feature/engineering-signal framing of the same residues).
relevance_note: an independent, methods-focused data point that a natural recombination process, not de novo engineering or single-lineage optimization, can plausibly account for the ACE2-binding residue pattern near the human/bat divergence.