Guillain-Barré syndrome and related diseases after influenza virus infection

We examined the clinical and serologic features of Guillain-Barré syndrome (GBS)-related diseases (GBSRDs), including GBS, Fisher syndrome (FS), and Bickerstaff brainstem encephalitis (BBE), after influenza virus infection (GBSRD-I) to reveal potential underlying autoimmune mechanisms.

We retrospectively investigated the presence of antiglycolipid antibodies against 11 glycolipids and the clinical features of 63 patients with GBSRD-I. Autoantibody profiles and clinical features were compared with those of 82 patients with GBSRDs after Campylobacter jejuni infection (GBSRD-C).

The anti-GQ1b seropositivity rate was significantly higher, whereas the GM1 and GD1a seropositivity rates were significantly lower in GBSRD-I compared with GBSRD-C. Anti-GQ1b and anti-GT1a were the most frequently detected antiglycolipid antibodies in GBSRD-I (both 15/63, 24%). Consequently, FS was more frequent in GBSRD-I than GBSRD-C (22% vs 9%, p < 0.05). In addition, as for GBS, cranial nerve deficits, sensory disturbances, and ataxia were more frequent in the cases after influenza infection (GBS-I) than in those after C. jejuni infection (GBS-C) (46% vs 15%, 75% vs 46%, and 29% vs 4%, respectively; all p < 0.01). Nerve conduction studies revealed acute inflammatory demyelinating polyneuropathy (AIDP) in 60% of patients with GBS-I but only 25% of patients with GBS-C (p < 0.01).

Anti-GQ1b antibodies are the most frequently detected antibodies in GBSRD-I. Compared with GBS-C, GBS-I is characterized by AIDP predominance and frequent presence of cranial nerve involvement and ataxia.