Mouse models of COVID-19 recapitulate inflammatory pathways rather than gene expression
Fig 5
Genetic background of K18-hACE2 mice affects disease progression.
(A) For each sample of the Suhrbier and Winkler datasets, the number of read pairs aligning to exon 9 and exon 2 of the Nnt gene are shown as green and purple bars, respectively. Nnt exon 9 is deleted in C57BL/6J mice. (B) Change in body weight over five days following SARS-CoV-2 infection is shown as a percentage of starting body weight for K18-hACE2 6J (Nnt-/-) and K18-hACE2 6J/6N (Nnt -/+) mice; p-values indicate significant difference between means at 3 and 4 dpi (Mann Whitney U tests, n = 5 per group). (C) Three disease score parameters (activity, posture and fur ruffling) over six days following SARS-CoV-2 infection are shown for K18-hACE2 6J and K18-hACE2 6J/6N mice. Statistics for 5 dpi for all 3 parameters by Kolmogorov-Smirnov tests (n = 5 per group). (D) Kaplan-Meier curves showing survival for K18-hACE2 6J and K18-hACE2 6J/6N mice following SARS-CoV-2 infection. Significance by log rank test (n = 5 per group). (E) Log10CCID50/g in brain, lung and nasal turbinate for K18-hACE2 6J and K18-hACE2 6J/6N mice 5 dpi with SARS-CoV-2. 6J data was derived from 2 independent experiments. Differences between K18-hACE2 6J and K18-hACE2 6J/6N mice for any tissue were not significance.