ArticlemSystems2026
Dysbiosis of fecal virome in pediatric Crohn's disease and its dynamic changes during infliximab therapy.
Article in mSystems, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
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Abstract
The gut virome is an emerging but underexplored component of the human microbiota, especially in pediatric Crohn's disease (CD). This study aimed to characterize the fecal virome in children with CD and evaluate its association with clinical response to infliximab (IFX) therapy. A total of 85 participants, including 60 pediatric CD patients and 25 healthy controls (HC), were recruited. Among the CD patients, 53 received ≥3 IFX infusions, 41 achieved remission (IFX-R), and 12 did not (IFX-NR). Viral-like particles in fecal samples were enriched and profiled by metagenomic sequencing, while bacterial communities were assessed via 16S rRNA gene sequencing. Pediatric CD patients exhibited significantly reduced viral richness and altered viral community compared to HCs. Functional analyses revealed that CD patients exhibit a shift in fecal virome function from DNA repair to viral replication and assembly. Trans-kingdom correlations were disrupted in CD, particularly between IMPORTANCE: Crohn's disease (CD) in children poses a growing clinical challenge, with increasing incidence and variable response to biologic therapies such as infliximab (IFX). While gut bacterial dysbiosis has been extensively studied, the role of the gut virome in pediatric CD remains largely unexplored. This study provides the first longitudinal characterization of the fecal virome in children with CD undergoing IFX therapy. We reveal distinct viral community patterns, functional alterations, and virus-bacteria interactions in pediatric CD patients. Notably, integration of virome and bacteriome profiles enhances diagnostic accuracy, offering a promising avenue for predictive biomarker development. Furthermore, virome changes may be associated with the IFX treatment outcomes in children with CD. These findings highlight the gut virome as a critical but overlooked dimension of host-microbiome interactions in pediatric CD, with potential implications for personalized therapy and mechanistic understanding of treatment resistance.
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