Home Research Feeds Cervicovaginal microbiota dysbiosis correlates with HPV persistent infection

Cervicovaginal microbiota dysbiosis correlates with HPV persistent infectionOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-04

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
China
Sample Site
Uterine cervix
Species
Homo sapiens

What was studied?

Researchers compared the cervicovaginal microbiota of women with persistent HPV infection, transient HPV infection, and healthy women, using 16S rDNA sequencing. They also measured local immune markers and circulating immune cell populations across the three groups.

How was it studied?

Cervicovaginal samples underwent 16S rDNA sequencing analysis, with LEfSe used to identify microbial biomarkers (LDA score above 4). Interleukin-6 and TNF-alpha were measured in cervical secretions, and Regulatory T cells and myeloid-derived suppressor cells were quantified in peripheral blood.

What did they find?

Healthy and transient-infection women had a comparatively simple microbiota dominated by Firmicutes, while persistent infection showed a more complex community with higher Proteobacteria, Actinobacteria, Bacteroidetes and Fusobacteria (Firmicutes p=0.003, Proteobacteria p=0.018, Bacteroides p=0.005). Prevotella, Sphingomonas and Anaerococcus at genus level correlated with persistent infection, while Lactobacillus iners correlated with transient infection; 36 dysbiosis biomarkers were identified overall. Interleukin-6, TNF-alpha, Regulatory T cells and myeloid-derived suppressor cells were all significantly elevated in the persistent infection group.

Why it matters

The findings link cervicovaginal microbiota dysbiosis and local immune changes to HPV persistence, the key step toward cervical intraepithelial neoplasia and cervical cancer. This suggests microbiota profiling could help distinguish persistent from transient HPV infection earlier.

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