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Species tropism of bat and mammalian ACE with SARS-CoV-2 variants. Nazia Thakur (9904162) Joseph Newman (5638340) Dongchun Ni (15188356) Jeffrey Seow (9415776) Abigail L. Hay (25157576) Yeonjae Lee (12256119) Ayush Upadhyay (25157573) Babatunde E. Ekundayo (25157578) John A. Hammond (7431785) Thomas P. Peacock (6536120) Kelvin Lau (1847764) Katie J. Doores (346210) Dalan Bailey (193037) Microbiology Cell Biology Evolutionary Biology Environmental Sciences not elsewhere classified Ecology Immunology Biological Sciences not elsewhere classified Cancer Infectious Diseases Virology multiple bat coronaviruses g ., rc g ., civet clade 1 viruses restricted ace2 usage mammalian ace2 proteins g ., rhgb07 using monoclonal antibodies clade 1 sarbecoviruses div >< p determined host range converting enzyme 2 2 convalescent individuals ace2 ), via using binding assays antigenicity using sera related bat sarbecoviruses using sarbecoviruses host range clade 3 pangolin ), neutralising antibodies entry assays binding domain sarbecoviruses interact sarbecoviruses exhibited rodent ace2 like rhgb07 generalist ace2 related antigenicity zoonotic potential vitally important still evidence specialist </ shifting pattern robust evidence research indicates racoon dog novel structure largely maintained including human immunodominant target human primate generalist phenotypes generalist </ especially omicron entry phenotypes diverse panel continued evolution breakthrough infections (A) Schematic of the emergence of SARS-CoV-2 variants depicting the divergence of the B lineage variants, including those variants of concern that grew to global dominance (B.1, Alpha, Beta, Delta, Omicron [black lines]), and the Omicron subvariants [red lines], some of which emerged via recombination events (dotted lines). Heatmap showing the bat and mammalian ACE2 usage of SARS-CoV-2 variants with (B) the B.1, Alpha, Beta, Delta and BA.1 variants, or (E) BA.2 and its subvariants BA.4/5, XBB, XBB1.5, BA.2.86. Data are shown as the mean fold change in pseudotype entry (RLU) of 3 separate experiments, relative to human ACE2. (C) Structure of SARS-CoV-2 BA.1 (PDB 7XO7) with mutations listed compared to B.1. Zoomed images of the Spike protein for B.1 (PDB 6M0J) and BA.1 (PDB 7WBP), highlighting key residues at positions 417, 484, 493 and 501 and the resultant interactions with human ACE2. (D) Specific amino acids within the B.1 RBD were mutagenised to make the RBD more BA.1-like (K417N, E484A, Q493R or N501Y) (top panel), or within BA.1 RBD to make the RBD more B.1-like (N417K, A484E, R493Q or Y501N) (bottom panel), either by themselves or in combination. Entry of these mutants was tested with Rh. cornutus, Rh. pusillus, Rh. ferrumequinum, and L. Lyra ACE2s. Data is shown as log fold-change in pseudotype entry, with green bars indicating an increase in virus entry and blue bars a decrease in entry, relative to B.1 (top panel) or BA.1 (bottom panel), highlighted also in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.3003944#pbio.3003944.g004" target="_blank">Fig 4B</a>. The data underlying this Figure can be found in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.3003944#pbio.3003944.s017" target="_blank">S1 Data</a>. 2026-10-01T17:40:07Z Image Figure 10.1371/journal.pbio.3003944.g004 https://figshare.com/articles/figure/_p_Species_tropism_of_bat_and_mammalian_ACE_with_SARS-CoV-2_variants_p_/34047376 CC BY 4.0