@article{mbs:/content/journal/jgv/10.1099/jgv.0.001166, author = "Liu, Fang and Wang, Honglei and Du, Li and Wei, Zeyu and Zhang, Qiong and Feng, Wen-hai", title = "MicroRNA-30c targets the interferon–alpha/beta receptor beta chain to promote type 2 PRRSV infection", journal= "Journal of General Virology", year = "2018", volume = "99", number = "12", pages = "1671-1680", doi = "https://doi.org/10.1099/jgv.0.001166", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.001166", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", keywords = "IFNAR2", keywords = "PRRSV", keywords = "miR-30c", keywords = "IFN-I", abstract = "Porcine reproductive and respiratory syndrome (PRRS) is one of the most important diseases in pigs. MicroRNAs (miRNAs) have emerged as an important regulator of virus–host cell interactions and miR-30c has been found to facilitate PRRSV replication. Here, we found that the interferon-alpha/beta receptor beta chain (IFNAR2) was down-regulated, while miR-30c was up-regulated during HV (a highly pathogenic type 2 PRRSV strain) and CH-1a (a classic type 2 PRRSV strain) infection. Subsequently, using bioinformatics analysis, we predicted that the IFNAR2 was targeted by miR-30c. A luciferase assay verified that the 3′ UTR of IFNAR2 was targeted by miR-30c, as a mutation on either the target sequence or the miR-30c seed sequence reversed the luciferase activity. In addition, miR-30c and IFNAR2 mRNA were physically co-localized in RNA-induced silencing complex (RISC). Importantly, we showed that miR-30c also impaired the induction of IFN-stimulated genes (ISGs) by targeting IFNAR2. Our findings further reveal the mechanism of miR-30c promoting PRRSV replication.", }