Fig. 3

MLL5 deficiency inhibits RNA virus replication both in vitro and in vivo. a Flow cytometry analysis of GFP fluorescence intensity in WT (blue) and MLL5^−/− (red) HEK293T cells infected with VSV-GFP (MOI:0.1) for 20 h. WT HEK293T cells without infection served as a negative control (gray). Statistical results are shown at the bottom. b–d Six to nine weeks old WT or Mll5^−/− littermates (n = 6) were intravenously infected with VSV-GFP (1 × 10⁷ pfu/g). After 12 h, ELISA quantification of IFN-β, TNF-α and IL6 in sera (b). Expression of Ifn-β,Tnf-α and Il6 mRNA after infection in the liver (c) and lung (d). Gapdh served as a control. e Six to nine weeks old WT (n = 3) or Mll5^−/− littermates (n = 4) were intravenously infected with VSV-GFP (1 × 10⁷ pfu/g), and sera were collected at 12 and 24 h after infection for plaque assay. f Expression of Vsv-g mRNA at 12 h after infection in the liver (left) and lung (right) treated as in c and d. Gapdh served as a control. g Hematoxylin–eosin staining of the lung sections from WT and Mll5^−/− mice infected with VSV-GFP (1 × 10⁷ pfu/g) for 12 h. Scale bar, 200 μm. h Six to nine weeks old WT or Mll5^−/− littermates (n = 6) were intravenously infected with VSV-GFP (1 × 10⁶ pfu/g) and monitored every 24 h after infection. i 6–9 weeks-old WT or Mll5^−/− littermates (n = 8) were intravenously infected with VSV-GFP (2 × 10⁷ pfu/g) and monitored every 6 h after infection. Data were representative of three independent experiments with similar results (g) or were from three independent experiments (a–d, f) or two independent experiments (e, i) or one experiment (h). Data were analyzed by Student’s t-test (two-tailed) or log-rank (Mantel–Cox) test and were presented as mean ± SD (*p < 0.05,**p < 0.01)