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.
Article first Published online 17 December 2013
*Institut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France;
†CNRS, UMR 8204, Lille, France;
‡Institut National de la Santé et de la Recherche Médicale, U1019, Team 7, Equipe FRM, Lille, France;
§Univ Lille Nord de France, Lille, France; and
‖Université Lille 2, Faculté de Médecine, CHRU de Lille, Laboratoire de Virologie EA3610, Loos-lez-Lille, France.
Reprints: Mathias Chamaillard, PhD, Institut Pasteur de Lille, 1, rue Professeur A. Calmette, 59496 Lille, France (e-mail: firstname.lastname@example.org).
The authors have no conflicts of interest to disclose.
Received October 29, 2013
Accepted November 19, 2013