Abstract
Porcine reproductive and respiratory syndrome (PRRS) is a disease caused by PRRS virus (PRRSV), which seriously harms the pig industry. Revealing the mechanism by which PRRSV inhibits immune response will help prevent and control PRRS. Here, we found that PRRSV-2 may hijack host miR-541-3p to inhibit host innate immune response. Firstly, this work showed that miR-541-3p mimics could facilitate the replication of PRRSV-2 and the results of the quantitative real time polymerase chain reaction (qRT-PCR) showed that PRRSV-2 could up-regulate the expression of miR-541-3p in MARC-145 cells. Since previous studies have shown that type I interferon could effectively inhibit the replication of PRRSV-2, the present work explored whether miR-541-3p regulated the expression of type I interferon and found that miR-541-3p could negatively regulate the transcription of type I interferon by targeting interferon regulatory factor 7 (IRF7). More importantly, PRRSV-2 infection could down-regulate the expression of IRF7 and over-expression of IRF7 could down-regulate the replication of PRRSV-2 in MARC-145 cells. In conclusion, PRRSV-2 infection up-regulated the expression of miR-541-3p to promote its replication in MARC-145 cells, since miR-541-3p can negatively regulate the transcription of type I interferon by targeting IRF7.
Highlights
Porcine reproductive and respiratory syndrome disease (PRRS), which is caused by PRRS virus (PRRSV) and is mainly characterized by reproductive failure of sows, high mortality of piglets and respiratory distress of pigs of all ages, is one of the most important diseases that seriously harm the pig industry
We found that miR-541-3p could promote the replication of PRRSV-2 since miR-541-3p could negatively regulate the transcription of type I interferon
In order to identify the target mRNA of miR-541-3p, the HEK 293T cells were prepared in 24-well plates and the cells were transfected with the pcDNA6.2-miR-541-3p or pcDNA6.2-Mut-miR-541-3p and psiCHECK-2-interferon regulatory factor 7 (IRF7)-3 -untranslated region (3 -UTR) or psiCHECK-2-Mut-IRF7-3 UTR, and, 24 h later, the cells were harvested for luciferase activity assay by using the dual-luciferase reporter assay system
Summary
Porcine reproductive and respiratory syndrome disease (PRRS), which is caused by PRRS virus (PRRSV) and is mainly characterized by reproductive failure of sows, high mortality of piglets and respiratory distress of pigs of all ages, is one of the most important diseases that seriously harm the pig industry. Due to the high frequency mutation of PRRSV gene, the gene recombination of different pedigrees/sublineages and the immunosuppression caused by PRRSV, there is still no effective vaccine to prevent PRRS. Other and our previous studies have shown that PRRSV infection has caused changes in miRNA expression profiles in MARC-145 cells and porcine alveolar macrophages (PAMs) and some PRRSV-regulated miRNAs have taken part in regulating the replication of PRRSV [12,13,14,15]. Our previous results of high-throughput sequencing of small RNAs from PRRSV-2-infected MARC-145 cells have shown that PRRSV-2 infection changes the expression profile of host miRNAs [15]. We selected several miRNAs which were regulated by PRRSV-2 infection to screen new miRNAs that could promote the replication of PRRSV-2. We found that miR-541-3p could promote the replication of PRRSV-2 since miR-541-3p could negatively regulate the transcription of type I interferon
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