Pacific premiere: 9/10 February 2026
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Atlantic replay: 11 February 2026
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Keynote talk by Dr. Simon Roux
Beyond microbes: multiomics reveals the influence of viruses on microbiomes
By Dr. Simon Roux, DOE Joint Genome Institute, Lawrence Berkeley National Laboratory, USA
Microbes are driving nutrient and energy transfers across the planet’s ecosystems, but do so under strong constraints exerted by viruses. Over the last decade, metagenomics revolutionized our ability to “see” viruses by providing large genome catalogs for uncultivated viruses, enabling a better characterization of virus-host interactions and their impact on microbiomes. I will present our latest work in this field, including new approaches to maximize the recovery and annotation of viral genomes from metagenomes, analysis of virus-host dynamics across diel cycles and seasons based on paired metagenomes and metatranscriptomes, and unexpected challenges in leveraging CRISPR spacer data to infer virus:host interactions.
Highlights
CFTR modulator therapy drives microbiome restructuring through improved host physiology in cystic fibrosis: the IMMProveCF phase IV trial
By Rebecca L. Knoll, University of California, San Francisco, USA
Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to impaired CFTR function, mucus accumulation, chronic infections, and inflammation. The triple combination elexacaftor/tezacaftor/ivacaftor (ETI) has transformed CF treatment by restoring CFTR function. However, how ETI-induced physiological improvements affect long-standing dysbiosis and pathogen colonization across microbiome habitats remains poorly understood. In this prospective longitudinal study (DRKS00023862), we analyzed sputum, throat, and stool microbiomes of pwCF (n = 35) before and after ETI initiation, alongside healthy controls (n = 49). The primary endpoint was longitudinal change in diversity, species richness, and microbial composition in the respiratory and intestinal microbiome, profiled by 16S rRNA gene sequencing. Secondary endpoints included changes in lung function, systemic and gastrointestinal inflammation. We show how improved CFTR function and direct antibacterial effects of ETI create a niche disadvantage for Staphylococcus in the sputum microbiome. Respiratory microbiome shifts were immediate, while gut changes emerged gradually. Escherichia abundance in stool, initially elevated in pwCF, decreased post-ETI and correlated with lower fecal calprotectin. These findings demonstrate that ETI can partially reverse CF-associated dysbiosis through improved host physiology. They offer insights into host-microbiome dynamics under therapeutic modulation and emphasize the need for confounder-aware models in complex clinical populations.
Diabetes alters the supragingival microbiome through plasma-to-saliva migration of glucose and fructose
By Atiko Sakanaka, The University of Osaka, Japan
Dental caries, a dysbiotic biofilm disease driven by polymicrobial acidogenesis, often coexists with type 2 diabetes (T2D). Previous studies suggest covarying relationships between circulating and salivary metabolites in patients with T2D. However, the role of hyperglycemia-induced saccharide migration from plasma to saliva in caries pathogenesis remains unclear. Here, we developed a novel method for untargeted metabolomics profiling of trace saliva from sublingual and submandibular glands, comparing this profile with those of plasma and whole saliva in participants with T2D (n = 31) and those with normoglycemia (n = 30). This comparison aimed to determine how circulating saccharide migration into the oral cavity and its subsequent microbial consumption are linked to dental caries. Additionally, shotgun metagenomic sequencing was combined with this analysis to investigate the cariogenic impact of circulating saccharide migration on the composition and function of supragingival biofilm using MetaPhlAn4 and HUMAnN3 pipelines.
The metabolomics profiles of glandular saliva showed intermediate dissimilarity between plasma and whole saliva, reflecting cardiometabolic traits more sensitively than whole saliva. Glucose and fructose showed a decreasing positive correlation with glycemic parameters in the order of plasma, glandular saliva, and whole saliva, suggesting systemic-to-oral migration and subsequent microbial consumption. Saccharide migration was more pronounced in participants with dental caries and plaque accumulation, coinciding with shifts in supragingival microbiota, including depletion of *Streptococcus sanguinis*, *Corynebacterium durum*, and *Rothia aeria*, and enrichment of *Streptococcus mutans*, *Veillonella parvula*, and *Actinomyces* sp. *oral taxon 448*. Glycolytic potential increased at the community level. Improved glycemic control reduced fructose migration and mitigated dysbiosis, decreasing fructose phosphotransferase abundance and shifting the *S. mutans*–*S. sanguinis* balance. Experimental validation demonstrated that fructose promotes *S. mutans* dominance over *S. sanguinis* in dual-species biofilms.
This study establishes saccharide migration as a metabolic driver of supragingival dysbiosis in T2D. The findings highlight the role of both glucose and fructose in caries pathogenesis and suggest that glycemic control may be an effective strategy as part of caries control.
Talks
Isolation, engineering and ecology of temperate phages from the human gut
By Jeremy Barr, Monash University, Australia
Large-scale metagenomic and data-mining efforts have revealed an expansive diversity of bacteriophages (phages) within the human gut1,2,3. However, functional understanding of phage–host interactions within this complex environment is limited, largely due to a lack of cultured isolates available for experimental validation. Here we characterize 134 inducible prophages originating from 252 human gut bacterial isolates using 10 different induction conditions to expand the experimentally validated temperate phage–host pairs originating from the human gut. Importantly, only 18% of computationally predicted prophages could be induced in pure cultures. Moreover, we construct a 78-member synthetic microbiome that, when co-cultured in the presence of human colonic cells (Caco2), led to the induction of 35% phage species. Using cultured isolates, we demonstrate that human host-associated cellular products may act as induction agents, providing a possible link between gastrointestinal cell lysis and temperate phage populations4,5. We provide key insights into prophage diversity and genetics, including a genetic pathway for domestication, finding that polylysogeny was common and resulted in coordinated prophage induction, and that differential induction can be influenced by divergent prophage integration sites. More broadly, our study highlights the importance of culture-based techniques, alongside experimental validation, genomics and computational prediction, to understand the biology and function of temperate phages in the human gut microbiome. These culture-based approaches will enable applications across synthetic biology, biotechnology and microbiome fields.
Strain displacement in microbiomes via ecological competition
By Erik Bakkeren, University of Calgary, Canada
Microorganisms commonly live in diverse communities where changes in composition can be critical for health, industry and the environment. Yet, what enables one strain to competitively replace another in these complex conditions remains poorly understood. Here we develop a mathematical model to determine general principles of strain displacement. Our modelling reveals that weak resource competition enables successful invasion while strong interference competition, for example, via antimicrobial production, enables successful displacement. We verify these predictions using in vitro assays with genetically engineered Escherichia coli. We then apply our principles to displace multidrug-resistant clinical isolates using strains that are equipped with a potent bacteriocin. Finally, we perform experiments with diverse human gut symbionts, which reveal that displacement relies on low resource competition not only between competing strains but also with the broader community, that is, limited nutrient blocking. These general rules for ecological success in microbial communities could be applied for targeted displacement of bacteria.
Human gut prophage landscape identifies a prophage-mediated fucosylation mechanism alleviating colitis
By Guanxiang Liang, Tsinghua University, Beijing, China
Functions of the human gut virome are little understood, particularly for the hyperabundant prophages integrated in prokaryotic genomes. Here we identified 254,273 prophage sequences in 47.7% of 289,232 human gut metagenomic genomes, significantly expanding the known taxonomic and functional diversity of prophages in the human gut microbiome. Analysis of 8503 gut metagenomic samples showed the ratios of lysogens (cells harboring prophages) to non-lysogens varied widely associated with age, health condition, and geography, with the latter linked to industrialization. Notably, the alterations of the prophage-encoded genes exhibited disease-specific patterns. For inflammatory bowel diseases, the prophage-encoded futC gene, encoding α-1,2-fucosyltransferase, was less prevalent in affected patients. This enzyme was experimentally validated to direct 2-fucosyllactose (2'-FL) biosynthesis in vitro. Here we show that 2'-FL could diminish colitis in mice induced by treatment with dextran sodium sulfate. Mechanistically, 2'-FL promoted maintenance of mucosal barrier integrity, leading to intestinal IgA secretion and intraepithelial CD4⁺CD8αα⁺ T cell development mediated by the gut microbiome. Together, our findings thus link lysogeny to human age, geography, and disease, and demonstrate an immunomodulatory mechanism of prophage-encoded genes in alleviating colitis.