State Key Laboratory of Agricultural Microbiology, Hongshan Laboratory and Key laboratory of Preventive Veterinary Medicine in Hubei Province, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Key Lab of Agricultural Animal Genetics, Breeding, and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan, 430070, China.
Virol Sin. 2022 Aug;37(4):591-600. doi: 10.1016/j.virs.2022.06.003. Epub 2022 Jun 7.
Pseudorabies virus (PRV), an etiological agent of pseudorabies in livestock, has negatively affected the porcine industry all over the world. Epithelial cells are reported as the first site of PRV infection. However, the role of host proteins and its related signaling pathways in PRV replication is largely unclear. In this study, we performed a quantitative phosphoproteomics screening on PRV-infected porcine kidney (PK-15) epithelial cells. Totally 5723 phosphopeptides, corresponding to 2180 proteins, were obtained, and the phosphorylated states of 810 proteins were significantly different in PRV-infected cells compared with mock-infected cells (P < 0.05). GO and KEGG analysis revealed that these differentially expressed phosphorylated proteins were predominantly related to RNA transport and MAPK signaling pathways. Further functional studies of NF-κB, transcription activator factor-2 (ATF2), MAX and SOS genes in MAPK signaling pathway were analyzed using RNA interference (RNAi) knockdown. It showed that only ATF2-knockdown reduces both PRV titer and viral genome copy number. JNK pathway inhibition and CRISPR/Cas9 gene knockout showed that ATF2 was required for the effective replication of PRV, especially during the biogenesis of viral genome DNA. Subsequently, by overexpression of the ATF2 gene and point mutation of the amino acid positions 69/71 of ATF2, it was further demonstrated that the phosphorylation of ATF2 promoted PRV replication. These findings suggest that ATF2 may provide potential therapeutic target for inhibiting PRV infection.
伪狂犬病病毒(PRV)是家畜伪狂犬病的病原体,它对全球养猪业造成了负面影响。上皮细胞被报道为 PRV 感染的第一部位。然而,宿主蛋白及其相关信号通路在 PRV 复制中的作用在很大程度上尚不清楚。在这项研究中,我们对 PRV 感染的猪肾(PK-15)上皮细胞进行了定量磷酸化蛋白质组学筛选。总共获得了 5723 个磷酸肽,对应 2180 种蛋白质,与 mock 感染细胞相比,PRV 感染细胞中 810 种蛋白质的磷酸化状态明显不同(P < 0.05)。GO 和 KEGG 分析表明,这些差异表达的磷酸化蛋白主要与 RNA 运输和 MAPK 信号通路有关。进一步使用 RNA 干扰(RNAi)敲低分析了 MAPK 信号通路中 NF-κB、转录激活因子-2(ATF2)、MAX 和 SOS 基因的功能。结果表明,只有 ATF2 敲低可降低 PRV 滴度和病毒基因组拷贝数。JNK 通路抑制和 CRISPR/Cas9 基因敲除表明,ATF2 是 PRV 有效复制所必需的,特别是在病毒基因组 DNA 的生物发生过程中。随后,通过 ATF2 基因的过表达和 ATF2 氨基酸位置 69/71 的点突变,进一步证明了 ATF2 的磷酸化促进了 PRV 的复制。这些发现表明,ATF2 可能为抑制 PRV 感染提供了潜在的治疗靶点。