Fig. 3: Infection of K18-hACE2 transgenic mice with ΔPRRA SARS-CoV-2.
From: Loss of furin cleavage site attenuates SARS-CoV-2 pathogenesis
a, Schematic of SARS-CoV-2 challenge, created with BioRender. b–f, Male and female mice were challenged with 103 PFU of wild-type (black) or ΔPRRA (blue) SARS-CoV-2, and evaluated for weight loss (n = 12 for both groups) (b), and viral RNA from the lung (c), nasal turbinate (d), nasal wash (e) and brain (f). At 2 days post-infection (dpi), n = 9 mice infected with wild type, 11 mice infected with ΔPRRA; at 7 dpi, n = 11 mice for both. N gene copies in the brain were measured at 7 dpi only. LOD, limit of detection. g, h, Lung function evaluated at 7 dpi using Flexivent mechanical ventilator to assess inspiratory capacity (g) and pressure–volume loop (h). n = 10 mice infected with wild type; n = 9 mice infected with ΔPRRA. i–k, Lung histopathology at 7 dpi from mock- (i), wild-type- (j) and ΔPRRA- (j) infected mice. Images are representative of lung sections from three mice in all cases. Scale bar, 250 μm. l, Chemokine analysis of mouse lung homogenates at 7 dpi, from mock-infected mice (white), or mice infected with wild-type (black) or ΔPRRA (blue) SARS-CoV-2. n = 8 for all groups. Data are mean ± s.e.m. P values from two-tailed Student’s t-test with unequal variance (b), Kruskal–Wallis Test for multiple comparisons (c–e, g, h), χ2 test (f) or a two-tailed Mann–Whitney test between wild-type and ΔPRRA (l).
