| Literature DB >> 33451106 |
Georges Tarris1,2, Alexis de Rougemont2, Maëva Charkaoui3, Christophe Michiels3, Laurent Martin1, Gaël Belliot2.
Abstract
Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is a multifactorial disease in which dietary, genetic, immunological, and microbial factors are at play. The role of enteric viruses in IBD remains only partially explored. To date, epidemiological studies have not fully described the role of enteric viruses in inflammatory flare-ups, especially that of human noroviruses and rotaviruses, which are the main causative agents of viral gastroenteritis. Genome-wide association studies have demonstrated the association between IBD, polymorphisms of the FUT2 and FUT3 genes (which drive the synthesis of histo-blood group antigens), and ligands for norovirus and rotavirus in the intestine. The role of autophagy in defensin-deficient Paneth cells and the perturbations of cytokine secretion in T-helper 1 and T-helper 17 inflammatory pathways following enteric virus infections have been demonstrated as well. Enteric virus interactions with commensal bacteria could play a significant role in the modulation of enteric virus infections in IBD. Based on the currently incomplete knowledge of the complex phenomena underlying IBD pathogenesis, future studies using multi-sampling and data integration combined with new techniques such as human intestinal enteroids could help to decipher the role of enteric viruses in IBD.Entities:
Keywords: Crohn’s disease; adenovirus; aichi virus; astrovirus; inflammatory bowel disease; norovirus; rotavirus; sapovirus; ulcerative colitis
Year: 2021 PMID: 33451106 PMCID: PMC7828589 DOI: 10.3390/v13010104
Source DB: PubMed Journal: Viruses ISSN: 1999-4915 Impact factor: 5.048