miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2
- PDF / 1,200,353 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 56 Downloads / 178 Views
RESEARCH
Open Access
miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2 Songbai Yang1, Yue Pei1, Xinyun Li2, Shuhong Zhao2, Mengjin Zhu2* and Ayong Zhao1*
Abstract Background: Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans. Pigs are important amplifier hosts of JEV. Emerging evidence indicates that host microRNAs (miRNAs) play key roles in modulating viral infection and pathogenesis. However, mechanistic studies delineating the roles of miRNAs in regulating host-JEV interactions remain scarce. Results: In this study, we demonstrated that miR-124 inhibited JEV replication in porcine kidney epithelial PK15 cells. Furthermore, using bioinformatics tools, we identified dynamin2 (DNM2), a GTPase responsible for vesicle scission, as a target of miR-124. Small interfering RNA (siRNA) depletion studies inicated that dynamin2 was required for efficient JEV replication. We also demonstrated that upregulation of miR-124 expression corresponded to decreased expression of its target, DNM2, in the JEV-infected PK15 cells. Conclusions: Overall, these results suggest the importance of miR-124 in modulating JEV replication and provide a scientific basis for using cellular miRNAs in anti-JEV therapies. Keywords: miR-124, JEV, DNM2, PK15, Porcine
Background Japanese encephalitis virus (JEV) is a mosquito-borne neurotropic virus that belongs to the family flaviviridae. JEV is mostly prevalent in eastern, southeastern and southern Asian countries where three billion people are at risk of contracting the disease [1]. A 2011 review estimated that the annual incidence was 1.8/100,000 and 5.4/100,000 for children 0-14 years old in 24 JEV endemic countries [2]. JEV is transmitted in an enzootic cycle between mosquito vectors and vertebrate hosts; humans contract JEV when bitten by an infected mosquito. Pigs act as amplifying hosts of JEV; therefore, the domestic pig was considered to be a risk factor in the transmission of the disease to humans [3, 4]. JEV is also one of the main causes of infectious reproductive failure in swine, and this has resulted in significant economic losses for the swine industry. The primary symptoms of pigs infected with JEV are fetal abortion and stillbirth in infected sows and * Correspondence: [email protected]; [email protected] 2 Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education & College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China 1 College of Animal Science and Technology, Zhejiang A&F University, Lin’an, Zhejiang 311300, China
aspermia in boars [5, 6]. In order to elucidate the pathogenesis of JEV in pigs, numerous studies on JEV have been conducted in PK-15 cells, a porcine kidney epithelial cell line, which have a similar susceptibility as skin epithelial cells to JEV [7–9]. Therefore, PK-15 cells are a good model in which to evaluate the host response to JEV infection. MicroRNAs (miRNAs) are small non-coding
Data Loading...
