BACKGROUND: We identified predominant vaginal microbiota communities, changes over time, and how this varied by HIV status and other factors in a cohort of 64 women. METHODS: Bacterial DNA was extracted from reposited cervicovaginal lavage samples collected annually over an 8-10 year period from Chicago Women's Interagency HIV Study participants: 22 HIV-negative, 22 HIV-positive with stable infection, 20 HIV-positive with progressive infection. The vaginal microbiota was defined by pyrosequencing of the V1/V2 region of the 16S rRNA gene. Scheduled visits included Bacterial vaginsosis (BV) screening; clinically detected cases were referred for treatment. Hierarchical clustering identified bacterial community state types (CST). Multinomial mixed effects modeling determined trends over time in CST, by HIV status and other factors. RESULTS: The median follow-up time was 8.1 years (range 5.5-15.3). Six CSTs were identified. The mean relative abundance (RA) of Lactobacillus spp. by CST (with median number of bacterial taxa) was: CST-1-25.7% (10), CST-2-27.1% (11), CST-3-34.6% (9), CST-4-46.8% (9), CST-5-57.9% (4), CST-6-69.4% (2). The two CSTs representing the highest RA of Lactobacillus and lowest diversity increased with each additional year of follow-up (CST-5, adjusted odds ratio (aOR) = 1.62 [95% CI: 1.34-1.94]; CST-6, aOR = 1.57 [95 CI: 1.31-1.89]), while the two CSTs representing lowest RA of Lactobacillus and higher diversity decreased with each additional year (CST-1, aOR = 0.89 [95% CI: 0.80-1.00]; CST-2, aOR = 0.86 [95% CI: 0.75-0.99]). There was no association between HIV status and CST at baseline or over time. CSTs representing lower RA of Lactobacillus were associated with current cigarette smoking. CONCLUSIONS: The vaginal microbial community significantly improved over time in this cohort of women with HIV and at high risk for HIV who had regular detection and treatment referral for BV. ; This is the copy of an article published in PLoS ONE PLoS One. 2015. 10(2). 10.1371/journal.pone.0116894. ; The Chicago WIHS-I-IV was funded by the National Institute of Allergy and Infectious Diseases, UO1-AI-34994 (PI: Mardge H. Cohen MD) and cofunded by the National Cancer Institute and the National Institute on Drug Abuse. This WIHS substudy was funded by an American Recovery and Reinvestment Act (ARRA) NIAID supplement to the Chicago WIHS (ARRA PI: G. Spear). The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.