Fig. 8: D-dimer levels in various tissues following infections of SARS-CoV-2 and variants. | Nature Communications

Fig. 8: D-dimer levels in various tissues following infections of SARS-CoV-2 and variants.

From: SARS-CoV-2 B.1.1.7 (alpha) and B.1.351 (beta) variants induce pathogenic patterns in K18-hACE2 transgenic mice distinct from early strains

Fig. 8

K18-hACE2 mice of both sexes (~1:1 ratio) were infected intranasally with USA-WA1/2020 (WA) of lineage A bearing 614D, New York-PV09158/2020 (NY) of lineage B.1.3 bearing 614G, USA/CA_CDC_5574/2020 (CA) of lineage B.1.1.7 or hCoV-19/South Africa/KRISP-EC-K005321/2020 (SA) of lineage B.1.351 at indicated doses in an ABSL-3 biocontainment. (a) D-dimer levels in lung, liver, and brain homogenates at indicated days post infection (dpi). Results combining two independent experiments are shown. Data are expressed as mean ± s.e.m (n = 7–9 mice/time point/tissue). Dotted horizontal lines indicate the limit of detection. (b) Correlation matrix of tissue-specific D-dimer levels with viral loads by Pearson correlation analysis after the log transformation of the data. Individual Pearson correlation coefficient r values are shown; (c) Principal component analysis (PCA) of D-dimer levels shown in Fig. 8a. The two most significant principal components (PC1 + PC2 > 98%) separate WA (614D)/NY (614G) infected mice and CA (B.1.1.7)/SA (B.1.351) infected mice into two groups based on D-dimer levels; (d) The Variable Importance in Projection (VIP) scores for the D-dimer levels in lung, liver and brain that drive the differences between WA/NY and CA/SA infected mice. Bar length corresponds to relative importance.

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