单细胞转录组分析HSV-1从潜伏感染的树和小鼠三胞胎瘤中重新激活,揭示了不同的分子和细胞过程
Yunshuang Ye1, Erlin Wang1, Mengqiu Yin2
1State Key Laboratory of Genetic Evolution & Animal Models, Yunnan International Joint Laboratory of Zoonotic Viruses, Yunnan Key Laboratory of Biodiversity Information, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650201, China; Department of Neurosurgery, Songjiang Research Institute, Songjiang District Central Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201615, China.
Virologica Sinica
|February 14, 2026
概括
人们对简单疹病毒1型 (HSV-1) 再激活的理解不充分. 这项研究揭示了受感染细胞蛋白0 (ICP0) 可能是通过抑制体内自细胞的方法对HSV-1的重新激活至关重要.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 神经科学是一个神经科学.
背景情况:
- 简单疹病毒1型 (HSV-1) 在70%以上的人口中产生终身潜伏感染.
- HSV-1的重新激活会导致各种疾病,但潜在的分子机制仍然不清楚.
研究的目的:
- 研究HSV-1延迟-重新激活过渡的细胞和分子事件.
- 在小鼠和树模型中比较HSV-1延迟特征.
- 阐明感染细胞蛋白0 (ICP0) 在HSV-1再激活中的作用.
主要方法:
- 大量RNA测序和单细胞转录组分析是在从小鼠和树模型中感染的三角生殖腺 (TG) 上进行的.
- 在体内研究了HSV-1潜伏-再激活过渡.
- 使用ICP0缺乏的HSV-1菌株来评估病毒蛋白在活性化中的作用.
主要成果:
- 树表现出活跃的延迟,而小鼠表现出静止的延迟.
- HSV-1感染了表达生长激素和垂体激素的TG神经元子群.
- 树的HSV-1潜伏抑制了自;在小鼠中,它减弱了与单细胞相关的免疫监测.
- 一种缺乏ICP0的HSV-1菌株未能自发地从树的潜伏期中重新激活.
结论:
- 感染细胞蛋白0 (ICP0) 可能对自发的HSV-1再激活至关重要.
- 在体内,ICP0可能会抑制自,从而促进HSV-1的重新激活.
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