tetano
Editor, Senior Moderator
Neurol Sci
. 2020 Oct 2.
doi: 10.1007/s10072-020-04787-7. Online ahead of print.
HLA and immunological features of SARS-CoV-2-induced Guillain-Barr? syndrome
Gian Luigi Gigli[SUP] 1 2 3 [/SUP], Alberto Vogrig[SUP] 1 [/SUP], Annacarmen Nilo[SUP] 4 [/SUP], Martina Fabris[SUP] 5 [/SUP], Alessia Biasotto[SUP] 5 [/SUP], Francesco Curcio[SUP] 2 5 [/SUP], Valeria Miotti[SUP] 6 [/SUP], Carlo Tascini[SUP] 7 [/SUP], Mariarosaria Valente[SUP] 1 2 [/SUP]
Affiliations
Abstract
We report the clinical and immunological features in a case of SARS-CoV-2-induced Guillain-Barr? 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.
Keywords: Coronavirus; Covid-19; Cytokines; Guillain-Barr? syndrome; Interleukin-6; Interleukin-8; Neurological complications; Neurology; Polyradiculoneuropathy.
. 2020 Oct 2.
doi: 10.1007/s10072-020-04787-7. Online ahead of print.
HLA and immunological features of SARS-CoV-2-induced Guillain-Barr? syndrome
Gian Luigi Gigli[SUP] 1 2 3 [/SUP], Alberto Vogrig[SUP] 1 [/SUP], Annacarmen Nilo[SUP] 4 [/SUP], Martina Fabris[SUP] 5 [/SUP], Alessia Biasotto[SUP] 5 [/SUP], Francesco Curcio[SUP] 2 5 [/SUP], Valeria Miotti[SUP] 6 [/SUP], Carlo Tascini[SUP] 7 [/SUP], Mariarosaria Valente[SUP] 1 2 [/SUP]
Affiliations
- PMID: 33006723
- DOI: 10.1007/s10072-020-04787-7
Abstract
We report the clinical and immunological features in a case of SARS-CoV-2-induced Guillain-Barr? 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.
Keywords: Coronavirus; Covid-19; Cytokines; Guillain-Barr? syndrome; Interleukin-6; Interleukin-8; Neurological complications; Neurology; Polyradiculoneuropathy.