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Helicobacter pylori infection alters gut virome by expanding temperate phages linked to increased risk of colorectal cancer
  1. Shiqi Luo1,2,
  2. Jinlong Ru1,2,
  3. Mohammadali Khan Mirzaei1,2,
  4. Jinling Xue1,2,
  5. Xue Peng1,3,
  6. Anna Ralser4,
  7. Joshua Lemuel Hadi1,2,
  8. Raquel Mejías-Luque4,5,
  9. Markus Gerhard4,5,
  10. Li Deng1,2
  1. 1Institute of Virology, Helmholtz Center Munich - German Research Center for Environmental Health, Neuherberg, Germany
  2. 2Chair of Prevention of Microbial Infectious Diseases, Central Institute of Disease Prevention and School of Life Sciences, Technical University of Munich, Freising, Germany
  3. 3Faculty of Biology, Biocenter, Ludwig Maximilian University of Munich, Planegg-Martinsried, Germany
  4. 4Institute for Medical Microbiology, Immunology and Hygiene, TUM School of Medicine and Health, Department Preclinical Medicine, Technical University of Munich, Munich, Germany
  5. 5Munich Partner Site, German Centre for Infection Research, Munich, Germany
  1. Correspondence to Professor Li Deng, Institute of Virology, Helmholtz Center Munich German Research Center for Environmental Health, Neuherberg, Germany; li.deng{at}

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Colorectal cancer (CRC) has low survival rates and can be influenced by various factors, including genetics, lifestyle and an altered microbiome.1 Recent studies indicate that Helicobacter pylori infection may also play a role in CRC development.2 This is of significant concern as over half of the world’s population carries H. pylori, which can cause gastric inflammation and potentially lead to cancer.3

In a recent study,4 we demonstrated that H. pylori infection in Apc-mutant mice could accelerate tumour development by causing immune and epithelial changes that are linked to tumorigenesis. We observed similar changes in H. pylori-infected patients.4 In addition, we found that treating the infection with antibiotics such as clarithromycin, metronidazole and omeprazole, at an early stage of infection can eradicate H. pylori4 and reduce the tumour occurrence to a normal level.4 These findings revealed the mechanisms behind H. pylori-induced CRC and highlighted the importance of gut bacteria. Yet, the role of gut viruses, particularly bacteriophages or phages, was overlooked despite their key role in regulating bacterial diversity, metabolisms and their association with diseases such as CRC.5

Therefore, we profiled the viral communities in cecum, stool and intestinal wash samples from Apc-mutant mice infected with H. pylori, with and without antibiotic treatment, as well as untreated controls using ViroProfiler6 (figure 1A …

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  • Contributors Conceptualisation: SL, MKM, LD and MG; Software: JR and XP; Investigation, SL and JLH; Data curation, SL and JR; Writing: SL, MKM and LD; Funding acquisition, LD; Resources: AR and RM-L; Supervision, JX, MKM and LD. Authors have approved the final draft of the manuscript.

  • Funding This work was funded by the Deutsche Forschungsgemeinschaft (DFG (German Research Foundation)) SFB1371/1-395357507 (project P09) to LD and MG and DFG project DE 2360/1-1 (Emmy Noether Program, project number 273124240) to LD, EU ERC StG-GA No. 803077 to LD.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; internally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.