Infectious origins of, and molecular mimicry in, Guillain-Barré and Fisher syndromes

Lancet Infect Dis. 2001 Aug;1(1):29-37. doi: 10.1016/S1473-3099(01)00019-6.


Guillain-Barré syndrome (GBS), characterised by limb weakness and areflexia, is the prototype of postinfectious autoimmune diseases, and Campylobacter jejuni is the most frequent antecedent pathogen. GBS subsequent to C jejuni enteritis is associated with a severe, pure motor axonal variant and IgG antibodies against GM1, GM1b, GD1a, or GalNAc-GDla, gangliosides expressed in human peripheral nerves. Lipopolysaccharides of C jejuni isolated from GBS patients have ganglioside-like epitopes. Cytomegalovirus is the most common viral antecedent infection. Patients with demyelinating GBS who have had a recent CMV infection have severe sensory deficits and anti-GM2 IgM antibody. CMV-infected fibroblasts express the GM2 epitope. Fisher syndrome (FS), characterised by ophthalmoplegia, ataxia, and areflexia, is a GBS variant associated with anti-GQ1b IgG antibody. GQ1b is enriched in the cranial nerves that innervate the extraocular muscles. Some patients develop FS after C jejuni infection, and the lipopolysaccharide present bears the GQ1b epitope. Molecular mimicry is a possible cause of GBS and FS.

Publication types

  • Review

MeSH terms

  • Animals
  • Campylobacter Infections / complications*
  • Campylobacter jejuni*
  • Chickenpox / complications
  • Cytomegalovirus Infections / complications*
  • Epstein-Barr Virus Infections / complications
  • Gangliosides / immunology
  • Guillain-Barre Syndrome / etiology*
  • Herpesvirus 3, Human
  • Humans
  • Immunoglobulin G / biosynthesis
  • Miller Fisher Syndrome / etiology
  • Molecular Mimicry*


  • Gangliosides
  • Immunoglobulin G