Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe reproductive failure in sows, respiratory diseases, and high mortality in piglets, which results in serious economic losses to the swine industry worldwide. Previous studies have described that PRRSV could suppress the host immune system and had antiapoptotic activity in its initial phase of infection. Polyinosinic-polycytidylic acid (poly I:C), a synthesized analogue of viral double-strand RNA, activates innate immunity responses and induces apoptosis in cells. Therefore, we performed miRNA transcriptome analysis of poly I:C–stimulated and PRRSV-infected porcine alveolar macrophages (PAMs) using deep sequencing technology, to compare the different miRNA profiles between the statuses of innate immune activation and inactivation. After sequencing, 267 known mature miRNAs and 64 novel miRNAs were observed in PAMs, and a total of 197 miRNAs were significantly differently expressed in poly I:C–stimulated PAMs, compared with mock control cells. Thirty-three of them were also significantly alerted in PRRSV-infected PAMs. This indicated that PRRSV only slightly alerted the miRNA expression profile of host cells compared with poly I:C–stimulated PAMs, which confirmed that PRRSV could suppress host innate immune responses during the early stages of infection. Among the differentially expressed miRNAs, we found that ssc-miR-27b-3p could significantly inhibit PRRSV RNA and protein replication in MARC-145 cells and PAMs. Its antiviral mechanism needs further research in the future.

中文翻译：

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聚I：C刺激和PRRSV感染的猪肺泡巨噬细胞的MicroRNA转录组分析。

猪繁殖与呼吸综合症病毒（PRRSV）导致母猪严重生殖衰竭，呼吸系统疾病以及仔猪高死亡率，这给全世界的养猪业造成严重的经济损失。先前的研究描述了PRRSV可以抑制宿主免疫系统，并且在感染的初始阶段具有抗凋亡活性。聚肌苷酸-聚胞苷酸（poly I：C）是病毒双链RNA的合成类似物，可激活先天免疫应答并诱导细胞凋亡。因此，我们使用深度测序技术对由聚I：C刺激和PRRSV感染的猪肺泡巨噬细胞（PAM）进行了miRNA转录组分析，以比较先天免疫激活和失活状态之间的不同miRNA图谱。测序后，与模拟对照细胞相比，在PAM中观察到267种已知的成熟miRNA和64种新颖的miRNA，并且在多聚I：C刺激的PAM中共表达了197种miRNA。在感染了PRRSV的PAM中，其中33个也得到了明显警告。这表明，与多聚I：C刺激的PAM相比，PRRSV仅稍微警告了宿主细胞的miRNA表达谱，这证实PRRSV在感染的早期可以抑制宿主固有的免疫反应。在差异表达的miRNA中，我们发现ssc-miR-27b-3p可以显着抑制MARC-145细胞和PAM中的PRRSV RNA和蛋白质复制。其抗病毒机制在未来需要进一步研究。C模拟的PAM与模拟对照组相比。在感染了PRRSV的PAM中，其中33个也得到了明显警告。这表明，与多聚I：C刺激的PAM相比，PRRSV仅稍微警告了宿主细胞的miRNA表达谱，这证实PRRSV在感染的早期可以抑制宿主固有的免疫反应。在差异表达的miRNA中，我们发现ssc-miR-27b-3p可以显着抑制MARC-145细胞和PAM中的PRRSV RNA和蛋白质复制。其抗病毒机制在未来需要进一步研究。C模拟的PAM与模拟对照组相比。在感染了PRRSV的PAM中，其中33个也得到了明显警告。这表明，与多聚I：C刺激的PAM相比，PRRSV仅略微提醒了宿主细胞的miRNA表达谱，这证实了PRRSV在感染的早期可以抑制宿主固有的免疫反应。在差异表达的miRNA中，我们发现ssc-miR-27b-3p可以显着抑制MARC-145细胞和PAM中的PRRSV RNA和蛋白质复制。其抗病毒机制在未来需要进一步研究。这证实了PRRSV可以在感染的早期抑制宿主固有的免疫反应。在差异表达的miRNA中，我们发现ssc-miR-27b-3p可以显着抑制MARC-145细胞和PAM中的PRRSV RNA和蛋白质复制。其抗病毒机制在未来需要进一步研究。这证实了PRRSV可以在感染的早期抑制宿主固有的免疫反应。在差异表达的miRNA中，我们发现ssc-miR-27b-3p可以显着抑制MARC-145细胞和PAM中的PRRSV RNA和蛋白质复制。其抗病毒机制在未来需要进一步研究。