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转录基因分析揭示了严重的宿主-病原体争端,在急性裂谷热病毒感染期间危害了恒温

Erick Bermúdez-Méndez^1,2,3,4, Paolo Angelino^3,4,5, Lucien van Keulen⁶

¹Department of Virology and Molecular Biology, Wageningen Bioveterinary Research, Lelystad, The Netherlands.

Journal of virology

|June 12, 2023

概括

裂谷热病毒 (RVFV) 在羊羔中的感染,通过降低代谢酶的调节,损害肝功能. 升高的LRP1表达可能会影响RVFV组织热带性,为病变发生提供了洞察力.

科学领域:

病毒学和病变发生学.
宿主-病原体相互作用
分子生物学分子生物学

背景情况:

裂谷热病毒 (RVFV) 是蚊子传播的病原体,会引起动物和人类的严重疾病,构成严重的公共卫生威胁.
尽管已知的*体外*干扰素反应,但RVFV病变的分子机制 *in vivo*,特别是宿主因子的参与,仍然不完全理解.
自然的RVFV感染是急性,病毒性迅速下降,需要更深入地了解自然宿主对宿主反应.

研究的目的:

为了研究 *in vivo* 主体转录特征,以应对羊羔的RVFV感染.
识别参与RVFV病变的宿主因素和基因调控网络.
阐明RVFV组织热带和器官功能障碍的分子基础.

主要方法:

用RNA测序 (RNA-seq) 技术分析了感染RVFV的羊的肝脏和脏组织中的宿主基因表达.
感染者和对照组之间的转录资料进行了比较,以确定不同表达的基因和途径.
研究了特定宿主因素,如LRP1,以确定它们在RVFV热带性和病变发生中的潜在作用.

主要成果:

证实,在RVFV感染期间,干扰素 (IFN) 介导的途径被强烈激活.
肝细胞亡与代谢酶的显著下调有关,导致肝功能受损和恒温.
肝脏中低密度脂蛋白受体相关蛋白1 (LRP1) 的基底表达升高与RVFV组织热带性有关.

结论:

RVFV感染通过降低基本代谢酶的调节,严重影响肝功能.
这项研究提供了对*in vivo*宿主反应的见解,强调了IFN通路和代谢失调的作用.
基底LRP1表达水平可能是RVFV组织热带的关键决定因素,进步了我们对其病原学的理解.

关键词:

在RNA-seqqq.裂谷热病病毒病毒主体-病原体相互作用病变的发生和发病.

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