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

Porcine hemagglutinating encephalomyelitis virus (PHEV) belongs to the order Nidovirales, family Coronaviridae, and genus Betacoronavirus. The virus causes vomiting and wasting disease (VWD) and/or encephalomyelitis in suckling piglets (Vijgen et al., 2006) . The virus was first isolated from the brains of suckling pigs with encephalomyelitis in Canada in 1962, after which the disease was reported in Japan, China, Argentina, and other countries (Greig et al., 1962; Mengeling et al., 1972; Hirai et al., 1974; Pensaert and Callebaut, 1974; Sasseville et al., 2001; Quiroga et al., 2008; Gao et al., 2011; Dong et al., 2014) . The mortality rate of PHEV-infected piglets under 3 weeks of age is almost 100%, whereas older pigs generally exhibit subclinical signs of infection. PHEV is a highly neurovirulent virus that invades the central nervous system (CNS) via the peripheral nerves, specifically focusing on microtubules and the intermediate filaments of nerve cells (Yagami et al., 1993; Hirano et al., 1995 Hirano et al., , 2004 Lyi et al., 2014; Foo and Chee, 2015) . Thus far, the mechanism for the neurotropism of PHEV remains unclear. Given that PHEV antigen-positive nerve cells are distributed widely in the cerebral cortex (Hirano et al., 1998) , a clarification of the pathogenesis in cortical neurons is expected to aid in understanding PHEV infectivity and propagation in the CNS.