[Skip to Content]
[Skip to Content Landing]
Views 679
Citations 0
Editorial
January 2017

Hepatitis E Virus and Guillain-Barré Syndrome

Author Affiliations
  • 1NeuroInfectious Disease Group, Department of Neurology, University of Colorado School of Medicine, Aurora
  • 2Department of Medicine (Infectious Diseases), University of Colorado School of Medicine, Aurora
  • 3Department of Immunology-Microbiology, University of Colorado School of Medicine, Aurora
JAMA Neurol. 2017;74(1):13-15. doi:10.1001/jamaneurol.2016.3651

A century ago when Guillain, Barré, and Strohl described the acute inflammatory polyneuropathic syndrome (Guillain-Barré syndrome [GBS]) for which they are still eponymously remembered, they noted that, “The pathogenesis of this radiculoneuropathic syndrome cannot be precisely defined. Although an infection or toxic insult should be considered, we have found no supporting evidence for either.”1(p316) Many patients with GBS have signs or symptoms consistent with an antecedent infection, generally involving the respiratory and/or gastrointestinal tracts.2,3 In about 50% of cases of GBS with a suspected infectious precipitant, a specific pathogen can be identified as a potential trigger of a presumably postinfectious immune-mediated process leading to disease. The strongest associations, based on epidemiological studies, involve bacteria (Camplylobacter jejuni and Haemophilus influenzae), mycoplasma (Mycoplasma pneumoniae), and viruses (cytomegalovirus [CMV] and Epstein-Barr virus [EBV]).2,3 A far larger list of pathogens may be involved in the pathogenesis of sporadic cases or produce clusters of GBS during outbreaks or epidemics, as recently suggested for the Zika virus.4

First Page Preview View Large
First page PDF preview
First page PDF preview
×