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部分功能耗尽的CD8+ T细胞可以促进短期的病毒抑制:对患有围产期HIV的儿童进行计算预测

Alexis Hoerter¹, Alexa Petrucciani¹, Fatma Marshed²

¹Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.

bioRxiv : the preprint server for biology

|September 26, 2025

概括

在患有围产期艾滋病毒的儿童中,T细胞的枯竭提供了短期的病毒控制,但导致过度的细胞死亡. 在幼儿中,早期的病毒抑制可以保持免疫反应,这对于儿科艾滋病毒治愈策略至关重要.

科学领域:

免疫学免疫学免疫学
计算生物学计算生物学
病毒学病毒学

背景情况:

在儿童中,周产期艾滋病毒感染与T细胞耗尽有关,其特征是抑制受体如PD-1,CD160和TIM-3的表达增加.
有限的数据存在于功能性病毒学后果的儿童群体这种免疫疲劳.

研究的目的:

在基于代理的模型 (ABM) 中计算整合T细胞分化,激活和耗尽的特征.
预测T细胞耗尽在肯尼亚儿童体外暴露艾滋病毒后对病毒控制的影响.
通过量化免疫功能障碍,为儿科艾滋病毒缓解和治疗策略提供信息.

主要方法:

利用来自肯尼亚患有围产期艾滋病毒的儿童和未暴露的对照者的免疫数据库.
开发了一种基于代理物的模型 (ABM),包括巨细胞,CD4+和CD8+T细胞,细胞因子和HIV动态.
模型包括病毒动态,免疫细胞激活/增殖/杀死,细胞因子/艾滋病毒降解,按病毒病和年龄 (<5或5-18岁) 分组.

主要成果:

尽管T细胞耗尽率高,但病毒活跃的儿童在新感染期间显示出较低的预测病毒载荷和受感染细胞,但细胞死亡增加.
病毒抑制的儿童>5年保持较低的病毒载荷与有限的细胞死亡,表明可持续的免疫反应.
病毒抑制的5岁以下儿童表现出与健康对照人群相似的免疫反应,这表明早期抑制可以保持抗病毒免疫力.
耗尽的CD8+ T细胞有助于杀死,增殖和激活病毒活性组,表明对短期控制的部分功能.
预测不同的细胞死亡模式:在病毒活跃组中CD8+ T细胞死亡占主导地位;在抑制/健康组中CD4+ T细胞和巨细胞死亡占主导地位.

结论:

在T细胞耗尽的儿科HIV中,短期的病毒控制与过度的炎症和细胞死亡有关.
在5岁以下的儿童中,早期的病毒抑制似乎可以保持抗病毒免疫反应.
部分功能性耗尽的CD8+ T细胞可以促进围产期艾滋病毒的短期病毒控制.
了解免疫功能障碍机制对于开发儿科HIV缓解和治愈策略至关重要.

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