细胞应激是由传播脑炎病毒触发的,并限制了PMJ2-R小鼠巨细胞系中病毒复制的可能性
Zuzana Beránková1, Ritesh Khanna1, Markéta Spěváková1
1Department of Medical Biology, Faculty of Science, University of South Bohemia, Branišovská 1760, CZ-37005 České Budějovice, Czech Republic.
Ticks and tick-borne diseases
|October 9, 2023
概括
性脑炎病毒 (TBEV) 感染引发宿主细胞应激反应,包括氧化和ER压力,限制病毒复制. 的唾液对这些压力路径的影响很小.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 病毒感染诱导宿主细胞应激反应以恢复平衡.
- 关于传染性脑炎病毒 (TBEV) 感染相关的压力路径的知识有限.
- 巨细胞是TBEV感染早期阶段的关键细胞.
研究的目的:
- 研究小鼠巨细胞中TBEV感染和细胞应激通路之间的相互作用.
- 确定诱导的压力如何影响TBEV复制.
- 分析唾液对TBEV感染细胞应激反应的影响.
主要方法:
- 暴露PMJ2-R小鼠巨细胞系的TBEV.
- 治疗应激诱导剂过氧化 (H2O2) 和突尼卡米辛 (TM).
- 测量反应性氧物种 (ROS),线粒体膜潜力 (MMP) 和未折叠蛋白质反应 (UPR) 标记物 (BiP,CHOP,IRE1).
- 对抗氧化酶基因表达的分析 (p62,Gclm,Hmox1).
- 唾液 (Ixodes ricinus) 对UPR的影响评估.
主要成果:
- 压力诱导剂H2O2和TM降低了TBEV复制.
- TBEV感染诱导间歇性ROS增加和MMP超极化.
- 观察到抗氧化酶基因 (p62,Gclm,Hmox1) 的暂时上调.
- TBEV感染激活了UPR的IRE1通路,并增加了BiP和CHOP基因表达.
- 的唾液只显示了UPR通路的边际增强.
结论:
- TBEV感染引发了氧化还原平衡的变化,并触发了细胞应激防御,包括抗氧化反应和UPR.
- 压力反应对TBEV复制产生负面影响.
- 的唾液对巨细胞中TBEV诱导的压力通路的影响有限.
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