4.4 Article

Bacterial vaginosis modifies the association between hormonal contraception and HIV acquisition

Journal

AIDS
Volume 32, Issue 5, Pages 595-604

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0000000000001741

Keywords

AIDS; bacterial vaginosis; HIV; hormonal contraception; injectable contraceptives; oral contraceptives; vaginal microbiota

Funding

  1. National Institute of Child Health and Development [NICHD R01 HD40125]
  2. National Institute of Mental Health [NIMH R01 66767]
  3. AIDS International Training and Research Program Fogarty International Center [D43 TW001042]
  4. Emory Center for AIDS Research [P30 AI050409]
  5. National Institute of Allergy and Infectious Diseases [NIAID R01 AI51231, NIAID R01 AI040951, NIAID R01 AI023980, NIAID R01 AI64060, NIAID R37 AI51231]
  6. US Centers for Disease Control and Prevention [5U2GPS000758]
  7. International AIDS Vaccine Initiative
  8. United States Agency for International Development (USAID)
  9. NICHD [1K23HD078153-01A1]

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Objective:To examine bacterial vaginosis as an effect modifier for the association between hormonal contraception and incident HIV infection.Design:Serodiscordant couples enrolled in an open longitudinal cohort in Lusaka, Zambia from 1994 to 2012. This analysis was restricted to couples with an HIV-positive man enrolled between1994 and 2002 when a quarterly genital tract examination and HIV testing was performed.Methods:Multivariate Cox models evaluated the association between contraceptive method and HIV-acquisition, stratified by time-varying bacterial vaginosis status.Results:Among 564 couples contributing 1137.2 couple-years of observation, bacterial vaginosis was detected at 15.5% of study visits. Twenty-two of 106 seroconversions occurred during intervals after bacterial vaginosis was detected [12 on no method/nonhormonal method (nonhormonal contraception), two on injectables, eight on oral contraceptive pills (OCPs)]. Unadjusted seroincidence rates per 100 couple-years for nonhormonal contraception, injectable, and OCP users, respectively, during intervals with bacterial vaginosis were 8.3, 20.8, and 31.0 and during intervals without bacterial vaginosis were 8.2, 9.7, and 12.3. In the bacterial vaginosis-positive model, there was a significant increase in incident HIV among those using injectables (adjusted hazard ratio, aHR 6.55, 95% CI 1.14-37.77) and OCPs (aHR 5.20, 95% CI 1.68-16.06) compared with nonhormonal contraception. Hormonal contraception did not increase the hazard of HIV acquisition in bacterial vaginosis-negative models. These findings persisted in sensitivity analyses whenever all covariates from the nonstratified model previously published were included, whenever other genital tract findings were excluded from the model and with the addition of condom-less sex and sperm on wet-prep.Conclusion:Future research should consider a potential interaction with bacterial vaginosis whenever evaluating the impact of hormonal contraception on HIV acquisition.

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