Bacterial co-infection as a catalyst in HPV-associated cervical carcinogenesis

Cervical cancer remains a preventable yet persistent global burden, with more than 660 000 new cases and 360 000 deaths reported in 2024. While high-risk HPV is the central driver of malignant transformation, growing evidence shows that bacterial co-infection can intensify HPV persistence and promote genomic instability. Meta-analyses now indicate that pathogens such as <i>Chlamydia trachomatis, Mycoplasma genitalium, Gardnerella vaginalis</i>, and diverse anaerobic microbiota markedly increase the risk of persistent HPV infection and cervical lesions. These microbes disrupt epithelial barriers, fuel chronic inflammation, and enhance the oncogenic activity of HPV E6/E7. Studies also show that Lactobacillus-depleted vaginal communities carry higher viral loads and increased CIN2⁺ progression. A 2024 review from sub-Saharan Africa further highlights frequent bacterial co-infections among HPV-positive women, particularly in settings with limited vaccination and screening. Together, these findings support a dual-pathogen model of cervical carcinogenesis and underscore the need to integrate microbiome-focused strategies into prevention efforts.