The Gut Virome in Gastrointestinal Cancers: Mechanisms, Biomarkers, and Translational Opportunities.
4 affiliations
- 1Department of Medicine and Technological Innovation, University of Insubria, 21100 Varese, Italy.
- 2Oncology Unit, Azienda Socio Sanitaria Territoriale Sette Laghi, 21100 Varese, Italy.
- 3Laboratory of Virology, National Institute for Infectious Diseases "Lazzaro Spallanzani" IRCCS, 00118 Rome, Italy.
- 4Laboratory of Medical Microbiology and Virology, University Hospital of Varese, Azienda Socio Sanitaria Territoriale Sette Laghi, 21100 Varese, Italy.
Abstract
The gastrointestinal tract contains a dense multi-kingdom ecosystem in which bacteria, fungi, archaea, viruses, the mucosa, and the immune system interact. Although cancer microbiome research has focused mainly on bacteria, the gut virome dominated by bacteriophages may influence gastrointestinal carcinogenesis by reshaping bacterial communities, transferring functional genes, modulating inflammation, and altering treatment response. The strongest evidence comes from colorectal cancer, where multiple cohorts show altered phage diversity, temperate-phage enrichment, disrupted phage-bacteria networks, and reproducible stool-based diagnostic signals. Emerging studies in pancreatic cancer, esophageal adenocarcinoma, hepatocellular carcinoma, and precursor lesions suggest that virome disruption extends beyond colorectal cancer, although evidence remains uneven. Classic oncogenic viruses, including Epstein-Barr virus and hepatitis viruses, provide complementary examples of direct viral carcinogenesis in digestive organs. Anelloviruses are widespread in healthy individuals and are not established causes of cancer, but their abundance and composition may reflect immune status, inflammation, tissue injury, and altered host viral ecology. Virome-related interventions remain clinically immature: fecal microbiota transplantation has reached small phase I/II studies in gastrointestinal cancers, whereas phage, fecal-filtrate, and fecal virome approaches remain preclinical or non-oncology; direct oncolytic viruses have reached late-phase testing. Major barriers include viral dark matter, specimen and assay heterogeneity, disease-related confounding, limited external validation, and weak causal evidence. Standardized, mechanistically anchored, multi-kingdom studies are needed to establish clinical utility.
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BibTeX
@article{ghidini2026virome,
title = {{The Gut Virome in Gastrointestinal Cancers: Mechanisms, Biomarkers, and Translational Opportunities.}},
author = {Michele Ghidini and Giuseppe Sberna and Luigi Pio Guerrera and Fabrizio Maggi and Federica Novazzi},
journal = {Viruses},
year = {2026},
month = oct,
doi = {10.3390/v18101131},
url = {https://europepmc.org/article/MED/42944051},
note = {CC BY},
}
RIS
TY - JOUR
TI - The Gut Virome in Gastrointestinal Cancers: Mechanisms, Biomarkers, and Translational Opportunities.
AU - Michele Ghidini
AU - Giuseppe Sberna
AU - Luigi Pio Guerrera
AU - Fabrizio Maggi
AU - Federica Novazzi
PY - 2026
DA - 2026/10/12
JO - Viruses
DO - 10.3390/v18101131
UR - https://europepmc.org/article/MED/42944051
AB - The gastrointestinal tract contains a dense multi-kingdom ecosystem in which bacteria, fungi, archaea, viruses, the mucosa, and the immune system interact. Although cancer microbiome research has focused mainly on bacteria, the gut virome dominated by bacteriophages may influence gastrointestinal carcinogenesis by reshaping bacterial communities, transferring functional genes, modulating inflammation, and altering treatment response. The strongest evidence comes from colorectal cancer, where multiple cohorts show altered phage diversity, temperate-phage enrichment, disrupted phage-bacteria networks, and reproducible stool-based diagnostic signals. Emerging studies in pancreatic cancer, esophageal adenocarcinoma, hepatocellular carcinoma, and precursor lesions suggest that virome disruption extends beyond colorectal cancer, although evidence remains uneven. Classic oncogenic viruses, including Epstein-Barr virus and hepatitis viruses, provide complementary examples of direct viral carcinogenesis in digestive organs. Anelloviruses are widespread in healthy individuals and are not established causes of cancer, but their abundance and composition may reflect immune status, inflammation, tissue injury, and altered host viral ecology. Virome-related interventions remain clinically immature: fecal microbiota transplantation has reached small phase I/II studies in gastrointestinal cancers, whereas phage, fecal-filtrate, and fecal virome approaches remain preclinical or non-oncology; direct oncolytic viruses have reached late-phase testing. Major barriers include viral dark matter, specimen and assay heterogeneity, disease-related confounding, limited external validation, and weak causal evidence. Standardized, mechanistically anchored, multi-kingdom studies are needed to establish clinical utility.
SN - 1999-4915
ER -