The researchers reported both community and species level differences which could predict disease severity, and tested these predictions in an independent cohort of 38 patients, helping to verify the validity of their results. Their models indicated that patients with more severe disease had multiple differences, such as reduced microbial diversity, including the depletion of 46 species-level taxa. This included depletion of Fusicatenibacter saccharivorans and Roseburia hominis, the former previously found to have a positive association with VO2max in men, increased butyrate production and reduced inflammation; both species were previously associated (inversely) to greater risk for long COVID. Eight taxa had increased relative abundance in the tool (such as Methanobrevibacter smithii and Bilophila wadsworthia), and multiple metabolic pathways were predicted to be affected, including reduced amino acid biosynthesis and short-chain fatty acid (SCFA) production pathways, as well as enrichment of primary bile acids and reduction of secondary bile acid metabolites.
This is not the first study to suggest that the microbiome plays a role in susceptibility to both severe disease following SARS-CoV-2 infection as well as persistent symptoms following infection, and that the modulation of microbial metabolites (e.g., bile acids, SCFAs, etc.) may be an important determinant of outcomes.