Fig. 7.

miR-33/33* agomirs predispose mice to viral infection in vivo. a Schematic model of the in vivo miR-33/33* experiment. Mice were primed with nc or miR-33/33* agomirs through tail vein injection for 3 constitutive days followed by VSV infection (i.p.) (10⁸ pfu per mouse, n = 8 per group). b Survival curve of 8-week-old, nc-, or miR-33/33* agomir-primed mice given intraperitoneal injection of VSV (10⁸ pfu/g) (n = 8 per group); *p < 0.05 (log-rank test). c Hematoxylin and eosin staining of lung sections from mice treated as in a 24 h i.p. Scale bar, 100 mm. d Determination of VSV loads in organs by TCID₅₀ assay from mice treated as in a 24 h i.p. e qRT-PCR analysis of VSV expression in organs from mice treated as in a 24 h i.p. f qRT-PCR analysis of Ifnβ mRNA expression in organs from mice treated as in a 24 h i.p. g ELISA of IFN-β production in serum from mice treated as in a 24 h i.p. h Schematic model of the regulatory role of miR-33/33* in the RIG-I signaling pathway wherein decreased Srebf2-miR-33/33* expression induced by type I IFNs produced in response to virus infection mediates positive feedback on type I IFN signaling to potentiate the antiviral state. *p < 0.05 (Student’s t test). Data are presented as the mean ± s.e.m. and are representative of three independent experiments.