Viral dysbiosis in children with new-onset celiac disease.

PLoS One

Department of Gastroenterology, Al Mofarreh PolyClinic, Riyadh, Kingdom of Saudi Arabia.

Published: February 2022

AI Article Synopsis

  • * This study analyzed the viral profiles from fecal and mucosal samples of 40 children with new-onset CeD and 39 healthy controls, finding distinct viral dysbiosis in the CeD group.
  • * Although specific viral species were found to be more or less abundant in the fecal samples of children with CeD, mucosal samples did not show significant associations, highlighting the complexity of viral interactions in gut health and the need for more research.

Article Abstract

Viruses are common components of the intestinal microbiome, modulating host bacterial metabolism and interacting with the immune system, with a possible role in the pathogenesis of immune-mediated diseases such as celiac disease (CeD). The objective of this study was to characterize the virome profile in children with new-onset CeD. We used metagenomic analysis of viral DNA in mucosal and fecal samples from children with CeD and controls and performed sequencing using the Nextera XT library preparation kit. Abundance log2 fold changes were calculated using differential expression and linear discriminant effect size. Shannon alpha and Bray-Curtis beta diversity were determined. A total of 40 children with CeD and 39 controls were included. We found viral dysbiosis in both fecal and mucosal samples. Examples of significantly more abundant species in fecal samples of children with CeD included Human polyomavirus 2, Enterobacteria phage mEpX1, and Enterobacteria phage mEpX2; whereas less abundant species included Lactococcus phages ul36 and Streptococcus phage Abc2. In mucosal samples however, no species were significantly associated with CeD. Shannon alpha diversity was not significantly different between CeD and non-CeD groups and Bray-Curtis beta diversity showed no significant separation between CeD and non-CeD samples in either mucosal or stool samples, whereas separation was clear in all samples. We identified significant viral dysbiosis in children with CeD, suggesting a potential role in the pathogenesis of CeD indicating the need for further studies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759644PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0262108PLOS

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