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. 2023 Jul 24;14:4454. doi: 10.1038/s41467-023-40126-y

Fig. 2. Residue F83 in PCDH1 is critical for Sin Nombre virus Gn/Gc: sEC1-2 binding.

Fig. 2

a Diagram of direct binding ELISA comparing sEC1-2(WT) and sEC1-2(F83L) capture of rVSVs. b Direct binding ELISA. rVSVs expressing ANDV, SNV, or HTNV Gn/Gc were added to sEC1-2(WT) or sEC1-2(F83L) coated ELISA plates. Means ± SD: n = 4 wells examined over two independent experiments. A, absorbance. c Diagram depicting competition ELISA comparing sEC1-2(WT) and sEC1-2(F83L) as competitive reagents. d Competition ELISA. rVSVs expressing ANDV or SNV Gn/Gc were pre-incubated with sEC1-2(WT) or sEC1-2(F83L) before added to sEC1-2(WT) coated ELISA plates. The ELISA signal was normalized to that obtained without competing sEC1-2. Means ± SEM: n = 7 wells examined over three independent experiments (ANDV), n = 4 wells examined over two independent experiments (SNV). e Diagram depicting infection-inhibition assay comparing sEC1-2(WT) and sEC1-2(F83L) as inhibiting reagents. f Infection-inhibition assay using sEC1-2(WT) and sEC1-2(F83L) to block infection (MOI of 0.1) of rVSVs bearing ANDV or SNV Gn/Gc on primary human endothelial cells (HUVECs). The infectivity of each virus was normalized to that obtained without sEC1-2. Averages ± SD: n = 6 wells examined over two independent experiments. (sEC1-2, soluble extracellular cadherin domains 1 and 2). Figures (a, c, e) were created with BioRender.com. Source data are provided as a Source Data file.