长期COVID中慢性炎症和改变的免疫反应与神经症状和加速衰老有关
Norina Tang1, Judith M Ford2, Kaitlyn Dal Bon2
1Department of Laboratory Medicine, San Francisco VA Health Care System, San Francisco, CA 94121, USA.
长期COVID的神经症状与持续的炎症和高血蛋白有关,即使在SARS-CoV-2感染数年后也是如此. 这些生物标志物可能表明加速衰老,并有助于诊断nLongC.
科学领域:
- 免疫学 免疫学 免疫学
- 神经学 神经学
- 遗传学 遗传学 是一个
背景情况:
- 一组感染SARS-CoV-2的个体经历了持续的神经症状 (nLongC).
- 导致nLongC和长期COVID-19后遗症的潜在生物机制尚不完全理解.
研究的目的:
- 调查持续性炎症标志物和与SARS-CoV-2感染后神经系统连续症相关的遗传因素.
- 确定潜在的生物标志物,以诊断和理解nLongC.的病理生理学.
主要方法:
- 在康复的COVID-19 (Cov) 个体中比较血蛋白水平和阿波利波蛋白E4 (APOE4) 基因载体,那些患有nLongC的人,和健康的对照 (HC).
- 分析了特定炎症标志物的纵向变化.
- 利用多种生物标志物模型,包括血蛋白,年龄,BMI和APOE4状态来评估诊断潜力.
主要成果:
- 与康复个体相比,患有nLongC的个体具有更高的APOE4基因患病率.
- 在Cov和nLongC组与HC组相比,四种血蛋白 (IL-1β,IL-8,GFAP,血素) 在Cov和nLongC组都升高.
- 在两组患者中,高IL-8和GFAP与年龄相关.
- 生物标志物的组合模型实现了区分组的AUC为0.81.
结论:
- 感染SARS-CoV-2可能会导致慢性,低级炎症状态,在急性疾病后持续很长时间.
- 持续性炎症和特定的生物标志物与nLongC相关,可能导致加速衰老.
- 已识别的生物标志物显示出有助于诊断和理解COVID-19长期神经效应的潜力.
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