ArticleInternational journal of cancer2019
A bacterial genotoxin causes virus reactivation and genomic instability in Epstein-Barr virus infected epithelial cells pointing to a role of co-infection in viral oncogenesis.
Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Genotoxic Bacteria and Oncogenic Viruses in Colorectal Cancer: Evidence, Gaps, and a Proposed Interaction Model.International journal of molecular sciences · 2026Review
- The microbiome-EBV axis in carcinogenesis bridges commensal influence and viral oncogenesis.Frontiers in immunology · 2026Review
- The role of probiotics in controlling oral biofilm formation and mitigating oral squamous-cell carcinoma risk.Archives of microbiology · 2025Review
- Awakening the sleeping giant: Epstein-Barr virus reactivation by biological agents.Pathogens and disease · 2024Review
- Antibodies to oral pathobionts and colon cancer risk in the CLUE I cohort study.International journal of cancer · 2023Article
- Oral Microbiota Alteration and Roles in Epstein-Barr Virus Reactivation in Nasopharyngeal Carcinoma.Microbiology spectrum · 2023Article
- Delivery, structure, and function of bacterial genotoxins.Virulence · 2022Review
- Review
- The human oral - nasopharynx microbiome as a risk screening tool for nasopharyngeal carcinoma.Frontiers in cellular and infection microbiology · 2022Article
- Influence of the FIV Status and Chronic Gingivitis on Feline Oral Microbiota.Pathogens (Basel, Switzerland) · 2020Article
- Oral and intestinal bacterial exotoxins: Potential linked to carcinogenesis.Progress in molecular biology and translational science · 2020Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have addressed the role of bacterial co-infection in viral oncogenesis using as model Epstein-Barr virus (EBV), a human herpesvirus that causes lymphoid malignancies and epithelial cancers. Infection of EBV carrying epithelial cells with the common oral pathogenic Gram-negative bacterium Aggregatibacter actinomycetemcomitans (Aa) triggered reactivation of the productive virus cycle. Using isogenic Aa strains that differ in the production of the cytolethal distending toxin (CDT) and purified catalytically active or inactive toxin, we found that the CDT acts via induction of DNA double strand breaks and activation of the Ataxia Telangectasia Mutated (ATM) kinase. Exposure of EBV-negative epithelial cells to the virus in the presence of sub-lethal doses of CDT was accompanied by the accumulation of latently infected cells exhibiting multiple signs of genomic instability. These findings illustrate a scenario where co-infection with certain bacterial species may favor the establishment of a microenvironment conducive to the EBV-induced malignant transformation of epithelial cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.