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. 2021 Jun 1;24(6):102678. doi: 10.1016/j.isci.2021.102678

Figure 1.

Figure 1

Msr1 contributes to VSV pathogenesis in mice

(A) Msr1 mRNA expression in various tissues of wild-type (WT, C57BL/6) and Msr1−/− mice. LOD, limit of detection; N = 3 mice per genotype.

(B and C) The survival curves (B) and disease scores (C) of WT and Msr1−/− mice challenged with 1×107 plaque-forming units (PFUs) per mouse of VSV by retro-orbital injection, N = 12 mice/genotype. p = 0.001 (log rank test), ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001, non-parametric Mann-Whitney U test. All the error bars: mean ± standard error of the mean (S.E.M.).

(D) The WT mice with paralyzed hindlimbs at day 6 after infection.

(E) Immunoblots of Msr1 protein expression in bone-marrow-derived macrophages (BMDMs) of WT, Msr1−/−, and Msr1+/− littermates. β-actin is a housekeeping control.

(F and G) The survival curves (F) and disease scores (G) of Msr1−/− and Msr1+/− littermates challenged with 1 × 107 PFU/mouse of VSV by retro-orbital injection, N = 6 mice/genotype. For percent survival, p < 0.01 (log rank test); for disease score, ∗∗p < 0.01, non-parametric Mann-Whitney U test. All the error bars: mean ± S.E.M.