title: Cellular microRNA miR-26a suppresses replication of porcine reproductive and respiratory syndrome virus by activating innate antiviral immunity.
abstract: Porcine reproductive and respiratory syndrome (PRRS) has caused large economic losses in the swine industry in recent years. Current PRRS vaccines fail to effectively prevent and control this disease. Consequently, there is a need to develop new antiviral strategies. MicroRNAs play critical roles in intricate host-pathogen interaction networks, but the involvement of miRNAs during PRRS virus (PRRSV) infection is not well understood. In this study, pretreatment with miR-26a induced a significant inhibition of PRRSV replication and remission of the cytopathic effect in MARC-145 cells, and this antiviral effect was sustained for at least 120 h. Luciferase reporter analysis showed that the PRRSV genome was not the target of miRNA-26a. Instead, RNA-seq analysis demonstrated that miR-26a significantly up-regulated innate anti-viral responses, including activating the type I interferon (IFN) signaling pathway and promoting the production of IFN-stimulated genes. These findings suggest that delivery of miR-26a may provide a potential strategy for anti-PRRSV therapies.
authors.affiliation: 1] Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China [2] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: Jia
authors.affiliation: CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
authors.forename: Yuhai
authors.initials: Y
authors.lastname: Bi
authors.affiliation: CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Clinical Laboratory, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Xie
authors.affiliation: Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China.
authors.forename: Hanchun
authors.initials: H
authors.lastname: Yang
authors.affiliation: 1] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China [2] University of Chinese Academy of Sciences, Beijing 100101, China.
authors.forename: Wenjun
authors.initials: W
authors.lastname: Liu
mesh_terms: D000818:Animals; D002460:Cell Line; D017930:Genes, Reporter; D054884:Host-Pathogen Interactions / Q000276:immunology; D007113:Immunity, Innate; D007370:Interferon Type I / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D010957:Plasmids / Q000235:genetics / Q000378:metabolism; D019318:Porcine Reproductive and Respiratory Syndrome / Q000276:immunology / Q000473:pathology / Q000821:virology; D019316:Porcine respiratory and reproductive syndrome virus / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D012367:RNA, Viral / Q000737:chemistry / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D017423:Sequence Analysis, RNA; D015398:Signal Transduction; D013552:Swine; D015854:Up-Regulation; D014779:Virus Replication
chemical_list: D007370:Interferon Type I; D035683:MicroRNAs; D012367:RNA, Viral