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MINI REVIEW article

Front. Oncol.

Sec. Cancer Molecular Targets and Therapeutics

Volume 15 - 2025 | doi: 10.3389/fonc.2025.1634388

This article is part of the Research TopicNovel Targets and Strategies for Developing Anti-Cancer Drug: Exploring the Role of Microorganisms in TumorsView all articles

HIV-Associated Gut Dysbiosis Drives Oncogenesis Through Metabolic-Immune Crosstalk: Mechanisms and Therapeutic Implications

Provisionally accepted
  • First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China

The final, formatted version of the article will be published soon.

HIV-induced gut microbiota dysbiosis perpetuates mucosal barrier disruption and systemic inflammation despite antiretroviral therapy (ART), creating a tumor-permissive microenvironment. This review synthesizes evidence linking HIV-associated microbial alterations to oncogenesis through three convergent metabolic axes: (1) butyrate deficiency impairing epithelial energy metabolism and anti-tumor immunity; (2) tryptophan metabolism dysregulation compromising gut barrier integrity via Akkermansia muciniphila depletion and Enterococcus-mediated phenylethylamine overproduction; and (3) vitamin B biosynthesis defects disrupting DNA repair and Th1/Th2 balance. Comparative profiling across HIV-associated malignancies-non-Hodgkin lymphoma, cervical cancer, hepatocellular carcinoma, and lung cancer-reveals conserved dysbiotic signatures: depletion of anti-inflammatory taxa (Bacteroidetes, Bifidobacterium) and expansion of proinflammatory genera (Proteobacteria, Shigella). These alterations activate NF-κB/STAT3 signaling, fostering IL-6/TNF-α-driven chronic inflammation. Emerging interventions, including Bifidobacterium-derived metabolites and butyrate supplementation, demonstrate potential to enhance immunotherapy efficacy and reverse chemoresistance. However, causal microbiota-tumor relationships remain unproven, and key AIDSdefining cancers (Kaposi sarcoma, anal carcinoma) lack microbial association studies. Prioritizing longitudinal multi-omics analyses, organoid models, and LMIC-focused clinical trials may advance microbiota-directed strategies for HIV-associated cancer prevention and treatment.

Keywords: HIV, Gut Microbiota, metabolite, tumor, immune

Received: 24 May 2025; Accepted: 04 Aug 2025.

Copyright: © 2025 Meng, Xu, 徐, Shen and Yue. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Qingquan Meng, First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China
Jngyu Yue, First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China

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