Exploring nasopharyngeal microbiota profile in children affected by SARS-CoV-2 infectionOriginal paper
What was studied?
This study examined the nasopharyngeal microbiota of children with COVID-19 compared to healthy controls. Nasal swabs were profiled by 16S rRNA targeted metagenomics. Analysis used QIIME 2, PICRUSt 2 for predicted function, and multiple machine learning classifiers. Swabs were taken at admission, at 72 hours to 7 days, and at discharge. Researchers tested whether a microbial signature marked infection and whether it changed over time or with SARS-CoV-2 viral load.
Who was studied?
The cohort was 71 children with confirmed SARS-CoV-2 infection and 59 age-matched healthy controls at Bambino Gesu Children's Hospital in Rome, Italy, sampled in 2020. A separate group of seven test-negative children was also included. COVID-19 patients had a median age of 6.5 years, with most disease classified as mild. Only 18 of 71 received antibiotics during admission. Viral load was stratified as high (22), medium (13), or low (15), with values unavailable for 21 patients.
What were the most important findings?
Infected children showed reduced alpha diversity and distinct community clustering versus controls. Their nasopharyngeal microbiota was enriched in Proteobacteria, Fusobacteriota, and Actinobacteria and depleted in Firmicutes, Bacteroidota, and Verrucomicrobiota. At family level, Staphylococcaceae, Streptococcaceae, Enterococcaceae, and Enterobacteriaceae rose, while Ruminococcaceae, Lachnospiraceae, Akkermansiaceae, Bacteroidaceae, and Bifidobacteriaceae fell (FDR less than 0.001). Streptococcus was a key genus marker. Machine learning classified patients from controls with up to 100 percent accuracy. The signature did not differ across time points or viral load levels.
What are the greatest implications of this study?
The results suggest pediatric COVID-19 carries a specific nasopharyngeal signature dominated by pathobionts and missing protective anaerobic commensals. This pattern was present from the first days of infection. Because diversity did not shift with viral load or during hospitalization, the microbiota change may be an early feature rather than a consequence of disease progression. The design is cross-sectional and cannot prove causation. The findings support studying nasal commensals as potential markers or modifiable factors in childhood respiratory infection.