miR-142-5p Disrupts Neuronal Morphogenesis Underlying Porcine Hemagglutinating Encephalomyelitis Virus Infection by Targeting Ulk1

Li, Zi; Lan, Yungang; Zhao, Kui; Lv, Xiaoling; Ding, Ning; Lu, Huijun; Zhang, Jing; Yue, Huiqing; Shi, Junchao; Song, Deguang; Gao, Feng; He, Wenqi

protein expression in PHEV-infected or healthy mice at 6 dpi ( Figure 9B) . The survival times of the antagomir-treated mice were significantly extended compared to PHEV-infected or control-treated mice (Figure 9C) , and they exhibited less prodrome (ruffled fur, hunched posture and standing walk), likely due to the lower miR-142-5p expression in the brain. At the same time, we found that PHEV proliferation was significantly restricted in the cerebral cortex of antagomirtreated mice at 5 dpi ( Figure 9D) . Immunofluorescence staining using PHEV mouse monoclonal antibodies showed that the number of positive PHEV-infected neurons was significantly reduced in the cerebral cortex and hippocampus of antagomir-treated mice (Figures 9E,F) . Taken together, these results suggested a potential role for the miR-142-5p antagomir in blocking PHEV neurovirulence in the host, which prolonged the survival times and decreased the prodromal signs.