Disrupted Vaginal Microbiota and Increased HPV Infection Risk Among Non-Vaccinated Women: Findings from a Prospective Cohort Study in Kazakhstan.

: Vaginal microbiota has emerged as an important factor influencing human papillomavirus (HPV) persistence and host immunity. While HPV infection is often transient, persistent infections with high-risk HPV genotypes significantly increase the risk of cervical carcinogenesis. Thus, this study aims to investigate the association between microflora/sexually transmitted infections (STIs) and HPV infection, with a focus on the prevalence of coinfection and the potential role of genital tract microecological disorders. : A prospective cohort study was conducted at a tertiary care center in Astana, Kazakhstan, between November 2024 and March 2025. A total of 396 non-pregnant women aged 18-45 years were enrolled during routine gynecological screening. Cervical samples were collected for high-risk HPV genotyping and the detection of 11 other vaginal microorganisms using real-time PCR. HPV-positive women were significantly younger and more likely to be single compared to HPV-negative participants. They also had fewer pregnancies and deliveries and were more likely to use barrier contraception. Among STIs, demonstrated a significant association with HPV infection (adjusted OR = 2.16, 95% CI: 1.15-4.05, = 0.017). Overall STI presence (adjusted OR = 2.16, = 0.017) and STI multiplicity (adjusted OR = 1.36 per additional STI, = 0.017) were also significantly associated with HPV positivity. Correlation analysis revealed a moderate association between and (ϕ = 0.39, < 0.001), suggesting shared ecological or transmission pathways. The findings highlight the relevance of specific vaginal pathogens, particularly and co-infection patterns in increasing the risk of HPV infection. These results underscore the importance of comprehensive STI screening and microbial profiling in cervical cancer prevention strategies, especially in populations with limited access to HPV vaccination. Further longitudinal and mechanistic studies are warranted to elucidate causal pathways and progression to cervical neoplasia.