# Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model

## TL;DR

This paper reviews how certain bacteria and viruses may work together to cause colorectal cancer, highlighting new insights into their interactions and potential for new treatments.

## Contribution

The paper proposes a novel interaction model between genotoxic bacteria and oncogenic viruses in colorectal cancer tumorigenesis.

## Key findings

- Genotoxic bacteria like Escherichia coli induce DNA damage and inflammation linked to cancer.
- Oncogenic viruses such as JCPyV and EBV are found in colorectal tissues and affect DNA repair processes.
- Bacterial genotoxins may enhance viral reactivation through DNA damage-induced signaling pathways.

## Abstract

Colorectal cancer (CRC) remains a significant global health burden, with growing evidence highlighting microbial contributions to its pathogenesis. Certain genotoxigenic bacteria, such as Escherichia coli, Campylobacter jejuni, and Helicobacter pylori, produce virulence factors that induce DNA damage, genomic instability, and chronic inflammation—key features of carcinogenesis. At the same time, viruses such as JC polyomavirus (JCPyV), considered potentially oncogenic, and established oncogenic viruses like Epstein–Barr virus (EBV) and human papillomavirus (HPV) have been detected in colorectal tissues and are linked to cell cycle regulation, apoptosis, and DNA repair through their viral proteins. Intriguingly, recent findings suggest that bacterial genotoxins may promote the reactivation or transcriptional activity of persistent viruses such as JCPyV and EBV, possibly through DNA damage-induced stress and activation of NF-κB- or ATM-dependent signaling pathways. Despite these advances, interactions between oncogenic viruses and bacteria within the colon microbiome remain underexplored. This review integrates current evidence and provides future perspectives for addressing potential genotoxic collaboration between bacteria and viruses that could contribute to colorectal tumorigenesis. Elucidating these interactions could reveal novel biomarkers and therapeutic targets for the prevention and treatment of CRC.