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.
Highlights
We investigated the exact role of the overexpression miR-26a during PRRS virus (PRRSV) infection and the miRNAs studied in previous reports[9,12] were used as controls
26a, miR-26a and control (miR-Ctr), miR-323, miR-654, miR-591, miR-608, miR-601, miR-509, miR-378, miR-939 and miR-491 were used to investigate the functions of miRNAs during PRRSV infection in susceptible cells (MARC-145)
PRRSV induced miR-26a expression in a dose-dependent manner (Fig. 1C). These data indicate that miR-26a is a PRRSV infection-responsive miRNA that can inhibit PRRSV replication in MARC-145 cells
Summary
Several reports show that cellular miRNAs can regulate viral infections by targeting viral genes[8,9,10,11,12] or host genes[13,14,15] Among these miRNAs, miR-26a inhibits H1N1 influenza A virus (IAV) replication may by binding to the conserved region of the PB1 gene[12]. We found that miR-26a inhibits PRRSV replication in MARC-145 cells This phenomenon was not related to miR26a binding to the PRRSV genome but was the result of up-regulating the innate immune response. Our results are consistent with the emerging notion that miRNAs are broadly involved in viral infection of mammalian cells and suggest that miR-26a may represent a potential therapeutic target for antiviral intervention of PRRSV infection
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