Department of Biotechnology, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.
Animal Genetics & Breeding Division, Department of Animal Resources Development, National Institute of Animal Science, Rural Development Administration, Cheonan, 31000, Republic of Korea.
Vet Immunol Immunopathol. 2021 Jan;231:110147. doi: 10.1016/j.vetimm.2020.110147. Epub 2020 Nov 18.
Porcine reproductive and respiratory syndrome virus (PRRSV) is a causative pathogen of PRRS, one of the most economically disastrous swine diseases. Non-structural protein 1 (NSP1) of PRRSV consists of NSP1α and NSP1β which exhibit papain like cysteine protease activity. Recent evidence demonstrates that PRRSV NSP1 may be participated in modulating host immunity, but very few host proteins were discovered as targets for NSP1. In this study, we used RNA-seq to investigate the functional role of PRRSV NSP1 in porcine alveolar macrophages, 3D4/31 cells. Compared to empty vector (mock) transfectant, NSP1, NSP1α, and NSP1β expressing 3D4/31 cells displayed a total of 60 genes, 63 genes, and 80 genes as differentially expressed genes (DEGs), respectively. Most of DEGs are involved in early inflammatory responses including interleukin (IL)-17 signaling pathway, chemokine signaling pathway, tumor necrosis factor (TNF)-α signaling pathway, and cell adhesion molecules. Interestingly, PRRSV NSP1 expression in 3D4/31 cells decreased mRNA transcripts of Fosb and Gdf15 known to be involved in host cell signaling or host cell protection during inflammation. Therefore, PRRSV NSP1 might block the signaling involved in host immune surveillance. Further study is required to define the mechanism on how PRRSV NSP1 protein represses mRNA transcripts of specific host genes.
猪繁殖与呼吸综合征病毒(PRRSV)是 PRRS 的病原体之一,是对猪最具破坏性的疾病之一。PRRSV 的非结构蛋白 1(NSP1)由 NSP1α 和 NSP1β 组成,它们具有木瓜样半胱氨酸蛋白酶活性。最近的证据表明,PRRSV NSP1 可能参与调节宿主免疫,但很少发现宿主蛋白作为 NSP1 的靶标。在这项研究中,我们使用 RNA-seq 来研究 PRRSV NSP1 在猪肺泡巨噬细胞 3D4/31 细胞中的功能作用。与空载体(mock)转染体相比,NSP1、NSP1α 和 NSP1β 表达的 3D4/31 细胞分别显示了总共 60 个、63 个和 80 个差异表达基因(DEGs)。大多数 DEGs 参与早期炎症反应,包括白细胞介素(IL)-17 信号通路、趋化因子信号通路、肿瘤坏死因子(TNF)-α 信号通路和细胞黏附分子。有趣的是,PRRSV NSP1 在 3D4/31 细胞中的表达降低了已知参与炎症期间宿主细胞信号转导或宿主细胞保护的 Fosb 和 Gdf15 的 mRNA 转录物。因此,PRRSV NSP1 可能阻断参与宿主免疫监视的信号。需要进一步研究来确定 PRRSV NSP1 蛋白如何抑制特定宿主基因的 mRNA 转录物的机制。