再激活的内源逆转录病毒促进蛋白质聚合物的传播
Shu Liu1,2, Stefanie-Elisabeth Heumüller1, André Hossinger1
1German Center for Neurodegenerative Diseases Bonn (DZNE), Venusberg Campus 1/ 99, 53127, Bonn, Germany.
Nature communications
|August 18, 2023
概括
内源逆转录病毒的激活加速了神经退行性疾病中蛋白质错折的传播. 用抗病毒药物向病毒蛋白可能会抑制蛋白质病种的细胞间传播.
科学领域:
- 神经生物学 神经生物学 神经生物学
- 分子生物学分子生物学
- 病毒学 病毒学
背景情况:
- 错误折叠的蛋白质的子样传播是神经退行性疾病的特征.
- 细胞间蛋白质聚合物的传播机制尚未完全理解.
- 内源逆转录病毒 (ERVs) 在神经退行性疾病 (如ALS和病) 中被上调.
研究的目的:
- 调查内源性逆转录病毒激活在蛋白质错折的类传播中的作用.
- 为了确定ERV是否影响蛋白质治疗种子的细胞间传播.
主要方法:
- 评估ERV上调对细胞培养中蛋白质聚合物扩散的影响.
- 测试向病毒包膜蛋白和病毒蛋白加工在抑制传播中的有效性.
- 评估来自不同类别的人体内源性逆转录病毒包裹对蛋白质病态种子传播的影响.
主要成果:
- 内源逆转录病毒的升级显著增加了细胞之间的蛋白质聚合物的传播.
- 病毒包膜蛋白或病毒蛋白加工的抑制减少了这种细胞间传播.
- 人类内源性逆转录病毒包裹增强了蛋白质治疗种子的传播,包括病态的Tau.
结论:
- 内源逆转录病毒在蛋白质错折疾病的进展中发挥作用.
- 针对ERV的抗病毒药物可能是抑制神经退行性疾病中蛋白质聚合物的传播的潜在治疗策略.
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