Fig. 3: Cell entry pathways of SARS-CoV-2 variants.
From: Phenotypic evolution of SARS-CoV-2 spike during the COVID-19 pandemic
a–c, Sensitivity of the panel of SARS-CoV-2 recombinant viruses to 10 μM each of camostat or E64d, either individually (a,b) or in combination (c), in AAT cells. The dotted line represents the relative viral load of DMSO-treated viruses set as 1.0. d,e, Sensitivity of SARS-CoV-2 viruses to 10 µM each of camostat or E64d in Calu-3 cells (d) or hNECs (e). f, Schematic representation of domain swap constructs between WT (lineage B) and A.30 spike. Full-length spike molecular model98 is based on PDB:6VXX ref. 5. g, Sensitivity of domain swap pseudoviruses (PV) to 10 µM camostat or E64d in AAT cells. Data are expressed relative to the DMSO-treated control for each virus. In a–e and g, data are mean ± s.e.m. of at least 3 independent experiments each performed in triplicate (n = 3). Statistical significance of differences between DMSO-treated and inhibitor-treated conditions was determined using one-sample t-test. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001.
