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DISC1通过AMPK-mTOR介导的自性来预防寨卡病毒感染和长期的神经损伤

Shengze Zhang^1,2, Haolu Zha^1,2, Qiqi Chen^1,2

¹School of Public Health (Shenzhen), Shenzhen Key Laboratory of Pathogenic Microbes and Biosafety, Shenzhen Campus of Sun Yat-sen University, Shenzhen, 518107, P.R. China.

Nature communications

|November 7, 2025

概括

精神分裂症1 (DISC1) 蛋白质中断减少了寨卡病毒 (ZIKV) 感染和先天性寨卡综合征. 自的DISC1激活保护ZIKV诱导的神经发育缺陷和认知衰退.

科学领域:

神经科学是一个神经科学.
病毒学病毒学
免疫学免疫学免疫学

背景情况:

精神分裂症中断1 (DISC1) 对神经元发育至关重要,并与精神疾病有关.
寨卡病毒 (ZIKV) 感染会提高DISC1的表达,但其在寨卡病毒病原和神经发育缺陷中的作用尚不清楚.

研究的目的:

研究DISC1在ZIKV感染,先天性寨卡综合征 (CZS) 和长期神经发育后果中的功能作用.
阐明DISC1影响ZIKV感染和相关病理的分子机制.

主要方法:

转录和蛋白质组分析以确定DISC1表达变化.
使用人类胎盘,神经质细胞和小鼠巨细胞进行体外研究.
在小鼠体内研究以评估ZIKV传播,胎儿结果和神经认知功能.
自途径的分析 (AMPKα,mTOR,LC3).

主要成果:

在各种细胞类型和小鼠模型中,DISC1显著减弱ZIKV感染.
DISC1减少了ZIKV向重要器官的传播,减轻了胎儿流产和子宫内生长限制.
DISC1与减少ZIKV诱导的大脑损伤和长期神经认知缺陷 (记忆,焦虑,社交) 有关.
DISC1通过AMPKα和mTOR途径激活自,并与LC3相互作用,以抑制ZIKV感染.

结论:

DISC1作为控制ZIKV感染的关键宿主因素.
DISC1在缓解先天性寨卡综合征和寨卡病毒诱导的神经认知衰退方面发挥着保护作用.
针对DISC1介导的自是一种潜在的治疗策略,可以对抗ZIKV.

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