Immunosenescence and microbial ecology in gastrointestinal and hepatobiliary infection-associated cancers

Infection-associated cancers of the gastrointestinal and hepatobiliary tract develop over years of interaction among persistent pathogens, injured tissues, anatomically distinct microbial communities, and a progressively remodeled immune system.This narrative review examines these interactions in Helicobacter pylori-associated gastric cancer, hepatitis B/C virus-associated hepatocellular carcinoma, and liver-fluke-associated cholangiocarcinoma, with microbially driven colorectal cancer used as a mechanistic boundary comparator.We distinguish immunosenescence from T-cell exhaustion and cellular senescence and evaluate microbial evidence according to anatomical compartment and evidentiary directness.Established human evidence is strongest for pathogen carcinogenicity and for the clinical benefit of pathogen eradication or suppression.By contrast, many proposed links between microbial function, immune aging, and cancer are supported mainly by animal models, experimental perturbation, or cross-sectional human studies.A complete longitudinal sequence in humans-from a defined compartment-specific microbial change to measurable immune aging and subsequent cancer progression-has not been demonstrated.Pathogen control and guideline-based surveillance therefore remain foundational, whereas microbiota-and immune-aging-directed interventions should be regarded as investigational and tested with compartment-matched functional biomarkers and clinically meaningful endpoints.