| Literature DB >> 30382935 |
Fang Liu1,2, Honglei Wang1,2, Li Du1,2, Zeyu Wei1,2, Qiong Zhang1,2, Wen-Hai Feng2,1.
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.Entities:
Keywords: IFN-I; IFNAR2; PRRSV; miR-30c
Mesh:
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Year: 2018 PMID: 30382935 DOI: 10.1099/jgv.0.001166
Source DB: PubMed Journal: J Gen Virol ISSN: 0022-1317 Impact factor: 3.891