Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Acta Neuropathol. 2023 Sep;146(3):387-394. doi: 10.1007/s00401-023-02612-x. Epub 2023 Jul 15.
Dysautonomia has substantially impacted acute COVID-19 severity as well as symptom burden after recovery from COVID-19 (long COVID), yet the underlying causes remain unknown. Here, we hypothesized that vagus nerves are affected in COVID-19 which might contribute to autonomic dysfunction. We performed a histopathological characterization of postmortem vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID.
自主神经功能紊乱显著影响了急性 COVID-19 的严重程度以及 COVID-19 (长新冠)康复后的症状负担,但潜在原因仍不清楚。在这里,我们假设 COVID-19 会影响迷走神经,这可能导致自主神经功能障碍。我们对 COVID-19 患者和对照者的死后迷走神经进行了组织病理学特征分析,并检测到了 SARS-CoV-2 RNA 以及主要由单核细胞组成的炎症细胞浸润。此外,我们进行了 RNA 测序,结果显示神经元、内皮细胞和施万细胞强烈的炎症反应与 SARS-CoV-2 RNA 载量相关。最后,我们对 323 例患者的临床队列进行了筛选,以检测迷走神经受累的临床表型,并发现重症 COVID-19 患者的无呼吸频率降低。我们的数据表明,SARS-CoV-2 诱导迷走神经炎症,继而导致自主神经功能障碍,这有助于严重疾病过程,并可能导致长新冠中观察到的自主神经功能紊乱。