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维生素D受体对于伪狂犬病病毒的复制至关重要

Lei Zeng^1,2,3, Shu-Yi Wang^1,2,3, Meng-Hua Du^1,2,3

¹College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, Henan, China.

|October 30, 2024

概括

伪狂热病毒 (PRV) 感染增加了维生素D受体 (VDR) 的表达,增强了的吸收和脂质合成. 这种VDR介导的途径促进了PRV的扩散,为PRV预防策略提供了新的目标.

科学领域:

病毒学病毒学
分子生物学分子生物学
生物化学生物化学

背景情况:

维生素D受体 (VDR) 调节生物功能的基因表达.
目前,VDR在伪狂犬病病毒 (PRV) 感染中的作用尚未被探索.
维生素D影响免疫功能和基因调节.

研究的目的:

调查VDR在PRV感染中的作用.
阐明VDR影响PRV增殖和宿主细胞过程的分子机制.
为了确定潜在的治疗目标,以预防PRV.

主要方法:

进行VDR淘汰和过度表达实验,以评估PRV的扩散.
在PRV感染期间分析VDR转录和VD3合成.
RNA测序 (RNA-seq) 用于识别VDR调节的途径.
的测量和路径分析 (PI3K/AKT/mTORC1,AMPK/mTORC1). 这些测量和路径分析包括:

主要成果:

VDR对PRV的扩散有积极的影响;VDR的淘汰会损害,而过度表达会促进它.
PRV感染上调调节VDR转录和VD3合成,这取决于p53的激活.
阻断VDR阻碍了PRV诱导的脂质合成.
VDR促进Ca2+吸收,激活PI3K/AKT/mTORC1和AMPK/mTORC1通路,这些通路对于脂质合成和PRV增殖至关重要.

结论:

PRV感染增强了VDR表达,导致Ca2+吸收增加和激活脂质合成通路 (PI3K/AKT/mTORC1和AMPK/mTORC1).
VDR在通过调节宿主脂质代谢来促进PRV扩散方面发挥着关键作用.
针对与VDR相关的信号通路,为PRV预防和治疗提供了一个潜在的策略.

关键词:

在 AMPK/mTORC1 中.在Ca2+中.在PI3K/AKT/mTORC1中.在 PRV 找 PRV.这是一个VDRVDR.脂质合成脂质合成在 p53 里,p53 是一个 p53 的代码.

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