巨细胞在长期COVID病理生理学的核心作用
Philip Mcmillan1, Anthony J Turner2, Bruce D Uhal3
1McMillan Research Ltd., 71-75 Shelton Street, Covent Garden, London WC2H 9JQ, UK.
International journal of molecular sciences
|January 10, 2026
概括
长期COVID或COVID的后急性后续可能源于持续的免疫失调和慢性巨细胞激活. 这种持续的炎症反应是由诸如尖端蛋白和表观遗传变化等因素驱动的,提供了新的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 病理生理学 病理生理学
背景情况:
- 后急性COVID (PASC) 或长期COVID的后续症状呈现出各种症状.
- 对长期COVID的现有解释是零碎的.
- 要了解长期COVID的潜在机制,需要一个统一的假设.
研究的目的:
- 为COVID (PASC) 后急性后果提出一个统一的假设.
- 确定慢性巨细胞激活是长期COVID的核心病理生理学.
- 阐明长期COVID中持续免疫反应的驱动因素.
主要方法:
- 对PASC和病毒综合征的现有文献的综述.
- 假设免疫失调的中心作用.
- 整合持久病毒元素和表观遗传修饰的证据.
主要成果:
- 长期COVID被假设为持续免疫失调的疾病.
- 慢性巨细胞激活被提出为基本的病理生理学.
- 持续的先天免疫反应是由持久的尖端蛋白,表观遗传印记和病毒储存所驱动的.
结论:
- 巨细胞激活是长期COVID病理学的核心.
- 这个框架允许个性化的风险评估.
- 建议针对长期COVID进行有针对性的干预和治疗再校准.
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