4.5 Article

Porcine reproductive and respiratory syndrome virus regulates lipid droplet accumulation in lipid metabolic pathways to promote viral replication

期刊

VIRUS RESEARCH
卷 333, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.virusres.2023.199139

关键词

PRRSV; Nf-kappa b signaling pathway; Lipid droplet; Lipid metabolism

类别

向作者/读者索取更多资源

Porcine reproductive and respiratory syndrome (PRRS) is a respiratory disease caused by porcine reproductive and respiratory syndrome virus (PRRSV). This study found that lipid metabolism and lipid droplets (LDs) play important roles in PRRSV replication. The study explored the mechanisms through which LDs affect PRRSV replication, and revealed the significance of the NF-kappa B signaling pathway regulation and LD accumulation in PRRSV replication.
Porcine reproductive and respiratory syndrome (PRRS) is a severe respiratory disease caused by porcine reproductive and respiratory syndrome virus (PRRSV) that can lead to the abortion of pregnant sows and decreased boar semen quality. However, the mechanisms of PRRSV replication in the host have not yet been fully elucidated. As lipid metabolism and lipid droplets (LDs) have been reported to play important roles in the replication of various viruses, we aimed to explore the mechanisms through which LDs affect PRRSV replication. Laser confocal and transmission electron microscopy revealed that PRRSV infection promoted intracellular LD accumulation, which was significantly reduced by treatment with the NF-kappa B signaling pathway inhibitors BAY11-7082 and metformin hydrochloride (MH). In addition, treatment with a DGAT1 inhibitor significantly reduced the protein expression of Phosphorylated NF-kappa B P65and PI kappa B and the transcription of IL-1 beta and IL-8 in the NF-kappa B signaling pathway. Furthermore, we showed that the reduction of the NF-kappa B signaling pathway and LDs significantly reduced PRRSV replication. Together, the findings of this study suggest a novel mechanism through which PRRSV regulates the NF-kappa B signaling pathway to increase LD accumulation and promote viral replication. Moreover, we demonstrated that both BAY11-7082 and MH can reduce PRRSV replication by reducing the NF-kappa B signaling pathway and LD accumulation. This study lays a theoretical foundation for research on the mechanism of PRRS prevention and control, as well as the research and development of antiviral drugs.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据