Flavinkins (@Flavinkins)

https://journals.asm.org/doi/10.1128/jvi.00958-22 It should be worth mentioning that unlike the N-linked glycome of other mammals, humans and cells of humans are unique in that they lacked either Neu5Gc or alpha-Gal. Bats contained the alpha-Gal epitope where other mammals contained both the Neu5Gc and the alpha-Gal epitope. https://www.sciencedirect.com/science/article/pii/S1931312820306806 An adaptation of Rhinolophid bats toward the loss of Neu5Gc synthesis (CMAH) is that they produce almost all alpha-Gal and almost no Neu5Ac on their glycocalyx. https://zenodo.org/record/5702700#.Ytew5BZ6slT Whatever HV6970 binds to, it likely abolished the ability of the S NTD to bind to alpha-Gal and favored Neu5Gc binding. Due to the anomalies found in BANaL-52 and RaTG13 (no bats in BANaL-52), and the observation that the SARS-CoV-2 S with HV6970 specifically showed greater tropism in VERO E6 cells compared to SARS-CoV S, in addition to human lung cells, and the fact that it is formed as HL6970 when GX/P2V is adapted in VERO E6, https://archive.ph/TrTW5 , and given that gaps are not counted toward identities when the SARS-CoV Urbani Spike was used as the reference for similarity alignment, the uniquely long NTD loops of the SARS-CoV-2 S and especially HV6970 should be considered a specific adaptation feature to Old-world non-human primate cells that contained Neu5Gc but not alpha-Gal. (As the NTD loop inserts are also deleted in VOCs, especially HV6970 indicating that it is not stable in humans (which don’t make either Neu5Gc or alpha-Gal) or any other species (other GX-CoVs don’t have HV6970/HL6970. Nor were GD-CoVs)). https://zenodo.org/record/6849652#.YteAXBZ6slR