Gui Liu1,2, Nelly R Mugo2,3, Elizabeth R Brown4,5, Nyaradzo M Mgodi6, Zvavahera M Chirenje7, Jeanne M Marrazzo8, Rachel L Winer1,9, Leila Mansoor10, Thesla Palanee-Phillips11,12, Samantha S Siva13, Logashvari Naidoo13, Nitesha Jeenarain13, Zakir Gaffoor13, Gonasagrie L Nair14, Pearl Selepe15, Clemensia Nakabiito16, Baningi Mkhize12, Brenda Gati Mirembe16, Marthinette Taljaard15, Ravindre Panchia17, Jared M Baeten1,2,18, Jennifer E Balkus1,2,4, Florian Hladik4,18,19, Connie L Celum2, Ruanne V Barnabas1,2,4,18. 1. Department of Epidemiology. 2. Department of Global Health, University of Washington, Seattle, Washington, USA. 3. Kenya Medical Research Institute, Nairobi, Kenya. 4. Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center. 5. Department of Biostatistics, University of Washington, Seattle, Washington, USA. 6. Clinical Trials Research Centre. 7. College of Health Sciences, University of Zimbabwe, Harare, Zimbabwe. 8. Department of Medicine/Division of Infectious Diseases, University of Alabama at Birmingham, Birmingham, Alabama. 9. Kaiser Permanente Washington Health Research Institute, Seattle, Washington, USA. 10. Centre for the AIDS Programme of Research in South Africa, University of KwaZulu-Natal, Durban. 11. Wits Reproductive Health and HIV Institute in Johannesburg. 12. Faculty of Health Sciences, University of Witwatersrand, Johannesburg. 13. South Africa Medical Research Council, Durban. 14. Desmond Tutu HIV Centre, University of Cape Town, Cape Town. 15. The Aurum Institute, Klerksdorp, South Africa. 16. Makerere University-Johns Hopkins University Research Collaboration, Kampala, Uganda. 17. Perinatal HIV Research Unit, Chris Hani Baragwanath Hospital, Soweto, South Africa. 18. Division of Allergy and Infectious Diseases, Department of Medicine. 19. Department of Obstetrics and Gynecology, University of Washington, Seattle, Washington, USA.
Abstract
OBJECTIVE: Vaccine-preventable human papillomavirus (HPV) infection is common, especially in sub-Saharan Africa where HIV risk is also high. However, unlike other sexually transmitted infections (STIs), HPV's role in HIV acquisition is unclear. We evaluated this relationship using data from MTN-003, a clinical trial of HIV chemoprophylaxis among cisgender women in sub-Saharan Africa. DESIGN: A case-control study. METHODS: We matched 138 women who acquired HIV (cases) to 412 HIV-negative controls. Cervicovaginal swabs collected within 6 months before HIV seroconversion were tested for HPV DNA. We estimated the associations between carcinogenic (high-risk) and low-risk HPV types and types targeted by HPV vaccines and HIV acquisition, using conditional logistic regression models adjusted for time-varying sexual behaviors and other STIs. RESULTS: Mean age was 23 (±4) years. Any, high-risk and low-risk HPV was detected in 84, 74 and 66% of cases, and 65, 55 and 48% of controls. Infection with at least two HPV types was common in cases (67%) and controls (49%), as was infection with nonavalent vaccine-targeted types (60 and 42%). HIV acquisition increased with any [adjusted odds ratio (aOR) 2.5, 95% confidence interval (95% CI) 1.3-4.7], high-risk (aOR 2.6, 95% CI 1.5-4.6) and low-risk (aOR 1.8, 95% CI 1.1-2.9) HPV. Each additional type detected increased HIV risk by 20% (aOR 1.2, 95% CI 1.1-1.4). HIV acquisition was associated with HPV types targeted by the nonavalent (aOR 2.1, 95% CI 1.3-3.6) and quadrivalent vaccines (aOR 1.9, 95% CI 1.1-3.2). CONCLUSION: HPV infection is associated with HIV acquisition in sub-Saharan African women. In addition to preventing HPV-associated cancers, increasing HPV vaccination coverage could potentially reduce HIV incidence.
OBJECTIVE: Vaccine-preventable human papillomavirus (HPV) infection is common, especially in sub-Saharan Africa where HIV risk is also high. However, unlike other sexually transmitted infections (STIs), HPV's role in HIV acquisition is unclear. We evaluated this relationship using data from MTN-003, a clinical trial of HIV chemoprophylaxis among cisgender women in sub-Saharan Africa. DESIGN: A case-control study. METHODS: We matched 138 women who acquired HIV (cases) to 412 HIV-negative controls. Cervicovaginal swabs collected within 6 months before HIV seroconversion were tested for HPV DNA. We estimated the associations between carcinogenic (high-risk) and low-risk HPV types and types targeted by HPV vaccines and HIV acquisition, using conditional logistic regression models adjusted for time-varying sexual behaviors and other STIs. RESULTS: Mean age was 23 (±4) years. Any, high-risk and low-risk HPV was detected in 84, 74 and 66% of cases, and 65, 55 and 48% of controls. Infection with at least two HPV types was common in cases (67%) and controls (49%), as was infection with nonavalent vaccine-targeted types (60 and 42%). HIV acquisition increased with any [adjusted odds ratio (aOR) 2.5, 95% confidence interval (95% CI) 1.3-4.7], high-risk (aOR 2.6, 95% CI 1.5-4.6) and low-risk (aOR 1.8, 95% CI 1.1-2.9) HPV. Each additional type detected increased HIV risk by 20% (aOR 1.2, 95% CI 1.1-1.4). HIV acquisition was associated with HPV types targeted by the nonavalent (aOR 2.1, 95% CI 1.3-3.6) and quadrivalent vaccines (aOR 1.9, 95% CI 1.1-3.2). CONCLUSION: HPV infection is associated with HIV acquisition in sub-Saharan African women. In addition to preventing HPV-associated cancers, increasing HPV vaccination coverage could potentially reduce HIV incidence.
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