Decoding norovirus infection in Crohn's disease

Inflamm Bowel Dis. 2014 Apr;20(4):767-70. doi: 10.1097/01.MIB.0000440613.83703.4a.

Abstract

Although a causing viral infectious agent remains untraceable in Crohn's disease, most recent genome-wide association studies have linked the FUT2 W143X mutation (resulting in asymptomatic norovirus infection) with the pathogenesis of Crohn's ileitis and with vitamin B12 deficiency (i.e., a known risk factor for Crohn's disease with ileal involvement). In line with these findings, host variations in additional genes involved in host response to norovirus infection (such as ATG16L1 and NOD2) predispose humans to Crohn's ileitis. One may therefore presume that asymptomatic norovirus infection may contribute to disruption of the stability of the gut microbiota leading to Crohn's ileitis. These paradigms highlight not only the need to revisit the potential transmissibility of Crohn's disease, but also potential safety issues of forthcoming clinical trials on human probiotic infusions in Crohn's ileitis by rigorous donors screening program.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alcohol Oxidoreductases
  • Asymptomatic Infections
  • Autophagy-Related Proteins
  • Caliciviridae Infections / complications*
  • Carrier Proteins / genetics
  • Crohn Disease / genetics*
  • Crohn Disease / virology*
  • Dysbiosis / genetics
  • Fucosyltransferases / genetics*
  • Genetic Predisposition to Disease
  • Humans
  • Ileitis / genetics*
  • Ileitis / virology*
  • Nod2 Signaling Adaptor Protein / genetics
  • Norovirus*

Substances

  • ATG16L1 protein, human
  • Autophagy-Related Proteins
  • Carrier Proteins
  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein
  • Alcohol Oxidoreductases
  • lactate-malate transhydrogenase
  • Fucosyltransferases
  • galactoside 2-alpha-L-fucosyltransferase