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<p><i>Human papillomavirus</i> (HPV) and <i>Chlamydia trachomatis</i> (CT) co-infection is increasingly recognized not as a mere coincidence, but as a synergistic partnership that accelerates oncogenic progression across multiple tissues. This review synthesizes existing evidence into a “central-peripheral” framework, positioning cervical cancer as the central, mechanistically well-established model of cooperation, while malignancies such as head and neck, ovarian, and breast cancers represent the emerging, though less substantiated, peripheral extensions. This synthesis delineates an emerging paradigm of bidirectional interplay: CT fosters a permissive microenvironment for HPV persistence by impairing host immunity and inducing chronic inflammation, while HPV oncoproteins promote tumorigenesis by disrupting tumor suppressor functions and reprogramming cellular metabolism. These resulting metabolic alterations in the host cell form the basis for the hypothesis of a metabolic co-dependency that may further reinforce CT persistence. The convergence of these pathogens on shared pathways, specifically immune evasion, genomic instability, and metabolic reprogramming, outlines a synergistic network. However, definitive proof of causality, particularly for the bidirectional effects in non-cervical cancers, remains constrained by methodological heterogeneity. Bridging these gaps requires future research to leverage immunocompetent co-infection models and multi-omics approaches. Elucidating the HPV-CT interactome supports a conceptual shift from a single-pathogen to a multi-pathogen oncogenesis model, which is pivotal for developing the next generation of precision prevention and therapy.</p>

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Synergism on Cancer Development of Human Papillomavirus and Chlamydia Trachomatis Co-Infection

  • 期刊论文

  • 发表日期：

    2026年1月20日

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  • Erqun Tang,
  • Yaqi Liao,
  • Zhenlei Wang,
  • Lanhua Zhao,
  • Mingxia Yang,
  • Youjun Chen,
  • Shuangyang Tang

摘要

Human papillomavirus (HPV) and Chlamydia trachomatis (CT) co-infection is increasingly recognized not as a mere coincidence, but as a synergistic partnership that accelerates oncogenic progression across multiple tissues. This review synthesizes existing evidence into a “central-peripheral” framework, positioning cervical cancer as the central, mechanistically well-established model of cooperation, while malignancies such as head and neck, ovarian, and breast cancers represent the emerging, though less substantiated, peripheral extensions. This synthesis delineates an emerging paradigm of bidirectional interplay: CT fosters a permissive microenvironment for HPV persistence by impairing host immunity and inducing chronic inflammation, while HPV oncoproteins promote tumorigenesis by disrupting tumor suppressor functions and reprogramming cellular metabolism. These resulting metabolic alterations in the host cell form the basis for the hypothesis of a metabolic co-dependency that may further reinforce CT persistence. The convergence of these pathogens on shared pathways, specifically immune evasion, genomic instability, and metabolic reprogramming, outlines a synergistic network. However, definitive proof of causality, particularly for the bidirectional effects in non-cervical cancers, remains constrained by methodological heterogeneity. Bridging these gaps requires future research to leverage immunocompetent co-infection models and multi-omics approaches. Elucidating the HPV-CT interactome supports a conceptual shift from a single-pathogen to a multi-pathogen oncogenesis model, which is pivotal for developing the next generation of precision prevention and therapy.