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. 2020 Oct 8;3:556. doi: 10.1038/s42003-020-01285-6

Fig. 1. MSR1 is critical for controlling CHIKV pathogenesis in mice.

Fig. 1

Eight-week old, sex-matched, C57BL/6 (WT) and Msr1 deficient (Msr1−/−) mice were infected with CHIKV. Quantitative RT-PCR analyses of a Msr1, CHIKV, type I IFN, ISG mRNA (n = 4 mice), b CHIKV loads in whole blood cells of WT and Msr1−/− mice (n = 8 mice per genotype). c Viremia presented as plaque-forming units (PFU) per ml serum (n = 8 mice per genotype). d Quantitative RT-PCR analyses of CHIKV loads in the ankle joints (n = 8 mice per genotype). e Fold changes in the footpad dimensions of infected mice over uninfected (day 0) (n = 8 mice per experimental group). f Representative micrographs of hematoxylin and eosin staining of ankle joints at 8 days after infection. n = 5 mice per genotype. B: bone, T: tendon, M: muscle. Magnification: ×200. g Arbitrary scores of ankle joint inflammation and damage using scales of 1 to 5, with 5 representing the worst disease presentation. n = 5 mice per genotype. h Quantitative RT-PCR analyses of the cellular viral loads in bone marrow-derived macrophages (BMDM) infected with CHIKV at a multiplicity of infection (MOI) of 10, n = 4. Each dot=one mouse/biological repeat, the small horizontal line: the median of the result. The data represent two independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 [b–d non-parametric t-test, e, g, h Student’s t-test].