多变异的宿主-病原体相互作用驱动异构的病毒分泌和CD8+ T细胞 控制流感病毒感染
Nicole Bruce1, Jordan J A Weaver1, Cailan Jeynes-Smith1
1Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN USA.
medRxiv : the preprint server for health sciences
|November 24, 2025
概括
由于病毒复制和CD8+T细胞反应的个体差异,流感感染的严重程度有所不同. 机械模型揭示了不同的感染模式,并突出了影响结果的宿主-病原体相互作用.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 数学生物学 数学生物学
背景情况:
- 流感病毒感染在个体之间在严重程度,病毒分泌和免疫反应方面表现出显著的变化.
- 这种流感感染结果异质性的潜在机制基础仍然不太清楚.
研究的目的:
- 研究病毒复制和CD8+T细胞反应的变化如何影响流感感染动力学和症状动态.
- 将多变量机械模型框架应用于人类挑战研究数据.
主要方法:
- 利用多变量机械模型框架来分析实验性感染H1N1流感病毒的个体的数据.
- 模拟病毒复制,CD8+T细胞反应,感染动力学和症状轨迹.
主要成果:
- 确定了六个不同的感染群体,受病毒剂量和复制率等因素的影响.
- 发现基线T细胞水平的影响最小,建议CD8+T细胞疗效与扩张之间的权衡.
- 在抗体阴性参与者中观察到潜在的再感染,并在症状报告中注意到主观性.
结论:
- 机制建模可以提高流感感染结果的可预测性.
- 人类内在的变异可能导致类似的感染轨迹,这凸显了流感中宿主-病原体相互作用的复杂性.
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