We report the clinical and immunological features in a case of SARS-CoV-2-induced Guillain-Barré syndrome (Si-GBS), suggesting that (1) Si-GBS can develop even after paucisymptomatic COVID-19 infection; (2) a distinctive cytokine repertoire is associated with this autoimmune complication, with increased CSF concentration of IL-8, and moderately increased serum levels of IL-6, IL-8, and TNF-α; (3) a particular genetic predisposition can be relevant, since the patient carried several HLA alleles known to be associated with GBS, including distinctive class I (HLA-A33) and class II alleles (DRB1*03:01 and DQB1*05:01). To the best of our knowledge, this is the first case of GBS in which SARS-CoV-2 antibodies were detected in the CSF, further strengthening the role of the virus as a trigger. In conclusion, our study suggests that SARS-CoV-2 antibodies need to be searched in the serum and CSF in patients with GBS living in endemic areas, even in the absence of a clinically severe COVID-19 infection, and that IL-8 pathway can be relevant in Si-GBS pathogenesis. Further studies are needed to conclude on the relevance of the genetic findings, but it is likely that HLA plays a role in this setting as in other autoimmune neurological syndromes, including those triggered by infections.

我们报告了一例 SARS-CoV-2 诱导的格林-巴利综合征 (Si-GBS) 病例的临床和免疫学特征，表明 (1) Si-GBS 即使在无症状 COVID-19 感染后也可发展；(2) 一种独特的细胞因子库与这种自身免疫并发症有关，脑脊液中 IL-8 浓度升高，血清 IL-6、IL-8 和 TNF-α 水平适度升高；(3) 特定的遗传易感性可能是相关的，因为患者携带了几个已知与 GBS 相关的 HLA 等位基因，包括独特的 I 类 (HLA-A33) 和 II 类等位基因 (DRB1*03:01 和 DQB1*05:01 ）。据我们所知，这是首例在脑脊液中检测到 SARS-CoV-2 抗体的 GBS 病例，进一步加强了病毒作为触发因素的作用。综上所述，我们的研究表明，即使在没有临床严重 COVID-19 感染的情况下，也需要在生活在流行区的 GBS 患者的血清和 CSF 中搜索 SARS-CoV-2 抗体，并且 IL-8 通路可能是相关的在 Si-GBS 发病机制中。需要进一步的研究来总结遗传发现的相关性，但 HLA 很可能在这种情况下发挥作用，就像在其他自身免疫性神经系统综合征中一样，包括由感染引发的那些。