Gut microbiota and serum metabolomics in children with human parainfluenza virus infection.

Abstract

Objective: Based on gut microbiota and serum untargeted metabolomics analyses, this study investigated changes in gut microbiota structure and serum metabolic profiles in children infected with human parainfluenza virus (HPIV). By integrating multi-omics data, we aimed to explore interactions between gut dysbiosis and serum metabolic disorders, and their potential roles in HPIV pathogenesis, to provide preliminary evidence for microbiota--targeted and metabolic intervention strategies.

Methods: Clinical data and laboratory results were collected from 230 hospitalized children (<14 years) with HPIV infection. Subsequently, 31 HPIV-infected children and 12 healthy controls were enrolled. Fecal samples were analyzed via 16S rRNA gene sequencing, and serum samples via liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based untargeted metabolomics, followed by integrated multi-omics analysis.

Results: Children with severe HPIV infection had longer hospital stays and higher frequencies of wheezing, tachypnea, dyspnea, and vomiting. HPIV infection was associated with gut dysbiosis: opportunistic pathogens (Anaerococcus, Peptoniphilus, Finegoldia) were enriched, while beneficial commensals (Blautia, Bifidobacterium, Faecalibacterium) were reduced. Metabolomics identified 579 upregulated and 211 downregulated metabolites, primarily enriched in alpha-linolenic acid, butanoate, glycerophospholipid, starch/sucrose, and glycine/serine/threonine metabolism pathways. Correlation analysis showed that enriched opportunistic pathogens positively correlated with pro-inflammatory lipids (e.g., acetoacetic acid, 3-hydroxybutyric acid) and negatively with protective metabolites (e.g., alpha-linolenic acid, sucrose, L-threonine), while Blautia showed opposite patterns. The four key genera and five metabolites demonstrated exploratory discriminatory capacity for HPIV infection (AUC: 0.81 and 0.98, respectively), serving as candidate biomarkers for further validation.

Conclusion: HPIV infection may be associated with gut microbiota dysbiosis and serum metabolic disturbances in children, potentially via the gut-lung axis, and these alterations may be involved in modulating pulmonary antiviral immune and inflammatory responses. This multi-omics study provides preliminary evidence for future research on prevention and treatment strategies targeting the gut microbiota or metabolic pathways in children with HPIV infection.