The underlying pathogenesis of neurological sequelae in post-COVID-19 patients remains unclear. Here, we used multidimensional spatial immune phenotyping and machine learning methods on brains from initial COVID-19 survivors to identify the biological correlate associated with previous SARS-CoV-2 challenge. Compared to healthy controls, individuals with post-COVID-19 revealed a high percentage of TMEM119⁺P2RY12⁺CD68⁺Iba1⁺HLA-DR⁺CD11c⁺SCAMP2⁺ microglia assembled in prototypical cellular nodules. In contrast to acute SARS-CoV-2 cases, the frequency of CD8⁺ parenchymal T cells was reduced, suggesting an immune shift toward innate immune activation that may contribute to neurological alterations in post-COVID-19 patients.

COVID-19 后患者神经系统后遗症的潜在发病机制仍不清楚。在这里，我们对最初的 COVID-19 幸存者的大脑使用多维空间免疫表型和机器学习方法，以确定与先前 SARS-CoV-2 挑战相关的生物相关性。与健康对照相比，COVID-19 后个体的典型细胞结节中组装有很高比例的 TMEM119 ⁺ P2RY12 ⁺ CD68 ⁺ Iba1 ⁺ HLA-DR ⁺ CD11c ⁺ SCAMP2 ⁺小胶质细胞。与急性 SARS-CoV-2 病例相比，CD8 ⁺实质 T 细胞的频率降低，表明免疫向先天免疫激活转变，这可能导致 COVID-19 后患者的神经系统改变。