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. 2016 Aug 15;113(36):10085–10090. doi: 10.1073/pnas.1601895113

Fig. 2.

Fig. 2.

Herpesvirus infection is augmented in arrhythmic Bmal−/− mice. (A) WT (n = 6) and Bmal1−/− (n = 5) female mice were intranasally infected with M3:luc MuHV-4 at ZT7. Extent and spread of infection was monitored by bioluminescence imaging. Representative images are shown with overlaid bioluminescence radiance measurements. (B) M3:luc MuHV-4 progressively disseminates from the nose to the SCLNs and is significantly higher in Bmal1−/− mice [mean ± SEM; nose two-way ANOVA (genotype × time postinfection): genotype effect, P = 0.0031; SCLN two-way ANOVA (genotype × time postinfection): genotype effect, P = 0.0348; post hoc t tests: *P < 0.05, **P < 0.01, ***P < 0.001]. See also Fig. S2A. (C) Male WT (n = 5) and Bmal1−/− (n = 6) mice were infected with CMV:luciferase (CMV:luc) herpes simplex virus 1 (HSV-1) by scarification of the left ear at ZT7. Extent and spread of infection was monitored and images presented as for A. (D) CMV:luc HSV-1 progressively disseminates from the left ear to the head and right ear and is significantly higher in Bmal1−/− mice [mean ± SEM; left ear two-way ANOVA (genotype × time postinfection): genotype effect, P = 0.0004; right ear two-way ANOVA (genotype × time postinfection): genotype effect, P = 0.0054; post hoc t tests: *P < 0.05, **P < 0.01]. See also Fig. S2E.