Dysbiotic Co-Factors in Cervical Cancer. How the Microbiome Influences the Development of Cervical Intraepithelial Neoplasia (CIN)

Abstract

Human papillomavirus (HPV) infection is a necessary but not sufficient condition for the development of cervical cancer. The dysbiotic shift in the cervicovaginal microbiome appears to be a major co-factor in carcinogenesis. New analytical methods, such as next-generation sequencing (NGS), can be used to detect all of the vaginal microorganisms present and therefore identify individual therapeutic options. The relationship of bacterial vaginosis and carcinogenesis, as well as possible indications for the use of microbiome analysis, will be discussed.

Keywords: CIN lesion; HPV infection; vaginal microbiome.

Fig. 1

Schematic representation of the influence of dysbiotic miscolonization on HPV infection, CIN progression and the development of cervical cancer. While the normal Lactobacillus-dominated vaginal microbiome (CST I, II, and V – “eubiosis”) allows clearance of HPV infection, loss of Lactobacillus dominance (CST IV) – and an increase in diversity – or dominance with L. iners (CST III) are associated with persistence of HPV, development and progression of CIN lesions, and the development of cervical cancer.

Abb. 1

Schematische Darstellung des Einflusses der dysbiotischen Fehlbesiedelung auf die HPV-Infektion, CIN-Progression und Entstehung des Zervixkarzinoms. Während das normale Lactobazillus-dominierte vaginale Mikrobiom (CST I, II und V – „Eubiose“) die Clearance der HPV-Infektion ermöglicht, hängt der Verlust der Lactobacillus-Dominanz (CST IV) – und Zunahme der Diversität – bzw. die Dominanz mit L. iners (CST III) mit der Persistenz von HPV, der Entstehung und Progredienz von CIN-Läsionen sowie der Entstehung von Zervixkarzinomen zusammen.