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伪狂热病毒UL13通过降低热冲击因子1的调节来启动炎症反应

Wen-Jing Zhang¹, Han Feng¹, Mei-Mei Zhang¹

¹National Key Laboratory of Agricultural Microbiology and Hongshan Laboratory, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.

|September 7, 2024

概括

伪狂热病毒 (PRV) 感染通过病毒蛋白UL13降低了热冲击因子1 (HSF1) mRNA水平. 这种操纵促进病毒复制和炎症,为阿尔法疹病毒感染提供了新的治疗点.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

伪病毒 (PRV) 是一个重要的猪病原体,造成经济损失.
阿尔法疹病毒感染可以影响宿主细胞反应,包括热冲击反应.
热冲击因子1 (HSF1) 是细胞应激反应的关键调节者.

研究的目的:

研究PRV蛋白UL13在感染期间调节HSF1中的作用.
阐明HSF1调制对PRV复制和宿主炎症反应的影响.
探索针对阿尔法疹病毒感染的HSF1通路的治疗潜力.

主要方法:

利用细胞培养模型和淘汰细胞系.
研究病毒蛋白相互作用和酶活性 (氨酸/氨酸蛋白激酶).
分析了基因表达 (mRNA水平) 和蛋白质酸化.
评估病毒复制率和炎症性细胞因子的产生 (IL-6,TNF-α,IL-1β).
检查了宿主免疫信号通路 (NF-κB,p38MAPK).

主要成果:

感染PRV会降低HSF1mRNA的水平.
病毒蛋白UL13的激酶活性对于HSF1mRNA的抑制和酸化至关重要.
尽管UL13降低了HSF1mRNA水平,但它增加了HSF1的活动.
缺陷或抑制HSF1显著降低了PRV复制.
HSF1的淘汰会加速NF-κB和p38MAPK的激活.
UL13调节细胞因子的产生,并有助于PRV诱导的病理.

结论:

PRV UL13利用其激酶活性来降低HSF1mRNA的调节,从而促进病毒复制和炎症.
HSF1在控制PRV复制和影响宿主免疫信号传递方面发挥着至关重要的作用.
准UL13-HSF1相互作用是针对PRV和其他alpha-herpesvirus的潜在治疗策略.

关键词:

阿尔法-疹病毒在HSF1中,它是HSF1.炎症炎症是一种炎症.UL13 UL13 UL13 UL13 UL13 UL13 UL13 UL13 UL13 UL13 UL13 UL13 在mRNA水平上.酸化的方法是:光化.

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