Fig. 3: Attenuated replication and pathogenesis of Omicron in K18-hACE2 transgenic mice.

Female and male K18-hACE2 transgenic mice (aged 6–8 weeks) were intranasally inoculated with 2 × 10³ plaque-forming units (p.f.u.) of Alpha, Beta, Delta, Omicron or WT SARS-CoV-2. Nasal turbinate and lung samples of the infected mice were collected at 2 or 4 d.p.i. to determine the viral burden. n = 6 (WT and Delta) and n = 8 (Omicron). The body weight and survival of the infected mice were monitored for 14 days. n = 7 (Omicron), n = 15 (WT), n = 9 (Alpha and Delta) and n = 12 (Beta). a, Viral RNA-dependent RNA polymerase (RdRp) gene copies were quantified using probe-specific RT–qPCR. b, sgE expression was quantified using probe-specific RT–qPCR. c, Infectious viral titres were quantified using plaque assays in VeroE6-TMPRSS2 cells. d, The expression of the inflammatory cytokine genes Cxcl10 and Ifng was quantified using RT–qPCR. e, f, The body weight (e) and survival (f) of mice infected with SARS-CoV-2 WT, Alpha, Beta, Delta or Omicron. Data are mean ± s.d. from the indicated number of biological replicates. The colour key in e also applies to f. Statistical significance was determined using one-way ANOVA (a–d), two-tailed Student’s t-tests (e) and log-rank (Mantel–Cox) tests (f); where multiple comparisons were performed among different groups, P values were adjusted using Tukey’s multiple-comparison test; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; NS, not significant. Data were obtained from two independent experiments. Each data point represents one biological replicate.

Source data