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

Our data demonstrated that functional mRNA repression by miR-142-5p is an important mechanism for abnormal neuronal development in primary cortical neurons during PHEV infection, and that Ulk1 are required for axonal elongation and plasticity. Because of miR-122 antagonism has been in phase II clinical studies as an HCV therapy (Lanford et al., 2010; Janssen et al., 2013) , which has shown that potently adjusting some microRNAs at a crucial level could lead to the rescue, or at least improvement, of nerve damage due to HCV. Thus, we presume that miR-142-5p antagonism is a potential novel strategy for PHEV therapeutic, which supported by antagonizing miR-142-5p resulted in PHEV replication restriction and prolonged survival times in PHEV-infected mice. However, the incompletely abolished viral replication indicated that there are other regulatory events in the physiological context of infection.