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Antimicrobial peptide resistance genes are found to be widespread in the gut microbiome but are exchanged at lower rates compared to antibiotic resistance genes, with functional compatibility between bacteria being important for gene exchange.
Integration of longitudinal gut metagenomic datasets from children in Finland, Estonia and Russian Karelia reveals high strain-level diversity, which consequently impacts the functional capabilities of the early life microbiome.
The Bacilluscereus enterotoxin haemolysin BL induces pore formation and activation of the NLRP3 inflammasome, leading to enhanced lethality during infection.
Using metabolomics and shotgun metagenomics on stool samples from individuals with and without inflammatory bowel disease, metabolites, microbial species and genes associated with disease were identified and validated in an independent cohort.
An age-dependent immunocompetent ferret model for severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) infection and pathogenesis recapitulates the clinical manifestations of human infections, including severe thrombocytopenia, reduced white blood cell counts and high fever with 93% mortality rate.
Two distinct pathways control inflammasome activation during Aspergillus fumigatus infection. The C-type lectin receptor (CLR) pathway activates MAPK and NF-κB signalling, whereas Toll-like receptor (TLR) signalling is activated through MyD88 and TRIF. Both pathways activate transcription factor IRF1, which induces antifungal effector IRGB10.
Hepatitis C virus (HCV) infection blunts induction of hepcidin expression by bone morphogenetic protein 6 (BMP6), probably via TNF-mediated downregulation of the BMP co-receptor HJV, while BMP6 regulates a gene repertoire reminiscent of type I IFN signalling. BMP6 and related activin proteins potently block replication of HCV, hepatitis B virus and Zika virus independently of IFN.
Clostridium difficile toxins TcdA and TcdB enhance pathogenesis by inducing vascular endothelial growth factor A (VEGF-A) production and promoting colonic vascular permeability.
Metagenomes from hydraulically fractured wells over time identified viral operational taxonomic units predicted to actively infect dominant bacteria, and in vitro experiments show that viral lysis of these hosts can release metabolites important for fermentation.
Autophagy-related proteins ATG16L1, ATG5 and ATG12 are required for plasma membrane repair and help to restrict Listeria monocytogenes toxin-mediated cell-to-cell spread.
The manipulation of expression of PfAP2-G, the master regulator of gametocytogenesis in malaria parasites, reveals that in addition to the canonical next cycle conversion route, sexual conversion can occur without additional replication (that is, within the same cycle).
A combination of genome sequencing of environmental archaeal isolates and experimental mating between Haloferax volcanii and Haloferax mediterranei shows that inter-species mating can induce the acquisition of CRISPR spacers, which modulate speciation.
Many enterovirus genomes harbour an upstream ORF (uORF) that is subject to strong purifying selection and encodes a protein (UP) that associates with membranes and facilitates virus release. UP-knockout echoviruses are attenuated at late stages of infection in human intestinal organoids.
Development of a structure-based method to predict potential ARDs present in human metagenomes indicates that resistance genes are rarely transferred within the human gut, and that individuals can be clustered into resistotypes.
Structural and functional characterization of H7-reactive monoclonal neutralizing antibodies from donors naturally infected with H7N9 influenza virus reveals overlapping epitopes around the receptor binding site of haemagglutinin and antigenic change in virus lineages isolated in 2013/14 versus 2016/17, indicating a need to update H7N9 vaccines.
Neutralizing murine monoclonal antibodies against the Eeastern equine encephalitis virus target the E2 glycoprotein, block infection at a post-attachment stage by inhibiting viral membrane fusion and protect mice from lethal challenge.
The synthesis of NPY and its receptor Y1R increases in lung phagocytes during severe influenza virus infection, leading to the induction of SOCS3 and impaired antiviral response and increased pro-inflammatory cytokine production.