human pathogen

Edge evidence

• human-adapted virulence factors enables human tissue tropism RO:0002327

  Human-adapted virulence factors enable preferential adhesion and growth in human tissues.

  • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports virulence factors as enablers of human tissue tropism.
• human tissue tropism enables human disease RO:0002327

  Tissue tropism supports establishment of human disease at specific anatomical sites.

  • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports tissue tropism as a determinant of human-disease pattern.
• human immune evasion enables human disease RO:0002327

  Evasion of human immunity supports sustained infection and disease.

  • DOI:10.1038/nrmicro1592 secretion systems Supports secretion-system-delivered effectors in human immune evasion.
• human disease manifests as human pathogen METPO:2007400

  Human disease manifests the human-pathogen trait.

  • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports the trait endpoint.
• type IV secretion system enables host cell manipulation RO:0002327

  Type IV secretion systems translocate protein effectors and toxins that manipulate host cells during infection.

  • DOI:10.1038/s41579-023-00974-3 T4SSs function as protein effector translocators delivering effectors or toxins; viable targets to thwart infection by pathogens.
• host cell manipulation enables human disease RO:0002327

  Effector-driven host cell manipulation supports establishment of human infection and disease.

  • DOI:10.1038/s41579-023-00974-3 Effector translocation enables host cell manipulation and infection by pathogens.
• horizontal gene transfer enables acquisition of virulence/host-adaptation genes RO:0002327

  HGT via plasmids, transduction, transposons, and IS elements enables acquisition of virulence and host-adaptation genes.

  • DOI:10.1093/femsre/fuae019 HGT via conjugation, transduction, transposons, IS elements can be associated with gain of genes facilitating host tropism and virulence factors.
• acquisition of virulence/host-adaptation genes enables human-adapted virulence factors RO:0002327

  Acquired genes contribute the human-adapted virulence factor repertoire underlying human pathogenicity.

  • DOI:10.1093/femsre/fuae019 Gene acquisition facilitates changes in host species tropism, including virulence factors enabling human-pathogenic lineages.
• within-host genetic diversification enables within-host adaptation and chronic infection RO:0002327

  Hypermutation, structural variation, and MGE/phage insertions generate diversity driving within-host adaptation.

  • DOI:10.1146/annurev-pathmechdis-051122-111408 Secondary mechanisms including hypermutation, structural variation, and MGE/phage insertions can increase pathogenicity and facilitate long-term persistence.
• within-host adaptation and chronic infection enables human disease RO:0002327

  Within-host adaptation increases pathogenicity and supports chronic human infection.

  • DOI:10.1146/annurev-pathmechdis-051122-111408 Within-host evolution can increase pathogenicity and facilitate long-term persistence in the host.
• biofilm formation enables treatment resistance and persistence RO:0002327

  Biofilm formation makes bacteria resistant to treatment and supports persistence.

  • DOI:10.3389/fmicb.2024.1370818 Bacteria can form biofilms, making them resistant to treatment.
• treatment resistance and persistence enables human disease RO:0002327

  Treatment resistance and persistence exacerbate the severity and duration of human infection.

  • DOI:10.3389/fmicb.2024.1370818 Biofilm-associated resistance to treatment contributes to infection severity and persistence.