State Key Laboratory of Veterinary Etiological Biology, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, China.
State Key Laboratory of Veterinary Etiological Biology, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, China.
Vet Microbiol. 2022 Dec;275:109595. doi: 10.1016/j.vetmic.2022.109595. Epub 2022 Nov 1.
MicroRNAs are small non-coding RNA that regulate host anti-viral immune response. In this study, we used high-throughput sequencing to identify miRNAs that were differentially expressed upon PRRSV infection in porcine alveolar macrophages. We observed that the expression level of miR-122 was decreased upon PRRSV infection. Over-expression of miR-122 remarkably suppressed PRRSV replication, while blockage of endogenous miR-122 enhanced PRRSV replication. Moreover, over-expression of miR-122 reduced the protein level of porcine suppressor of cytokine signaling 3 (SOCS3), a negative regulator of JAK-STAT signaling, resulting in enhanced production of type Ⅰ IFN. Further analysis revealed that miR-122 decreased the expression of SOCS3 at the post-transcription level by targeting the 3' UTR region of SOCS3 mRNA. In conclusion, this study demonstrates that the expression of miR-122 was reduced during PRRSV infection. miR-122 impaired PRRSV replication by promoting the production of type I interferon. Our study may provide new insights into understanding PRRSV immune evasion mechanisms.
微小 RNA 是调节宿主抗病毒免疫反应的小非编码 RNA。在这项研究中，我们使用高通量测序来鉴定在猪肺泡巨噬细胞中 PRRSV 感染时差异表达的 miRNA。我们观察到 miR-122 的表达水平在 PRRSV 感染后降低。miR-122 的过表达显著抑制了 PRRSV 的复制，而内源性 miR-122 的阻断增强了 PRRSV 的复制。此外，miR-122 的过表达降低了猪细胞因子信号转导抑制因子 3（SOCS3）的蛋白水平，SOCS3 是 JAK-STAT 信号的负调节剂，导致Ⅰ型 IFN 的产生增加。进一步分析表明，miR-122 通过靶向 SOCS3 mRNA 的 3'UTR 区域降低 SOCS3 的表达。总之，本研究表明 miR-122 的表达在 PRRSV 感染过程中降低。miR-122 通过促进 I 型干扰素的产生来损害 PRRSV 的复制。我们的研究可能为理解 PRRSV 免疫逃逸机制提供新的见解。
