Susan Hariri1, Nancy M Bennett2, Linda M Niccolai3, Sean Schafer4, Ina U Park5, Karen C Bloch6, Elizabeth R Unger7, Erin Whitney8, Pamela Julian9, Mary W Scahill10, Nasreen Abdullah11, Diane Levine12, Michelle L Johnson13, Martin Steinau14, Lauri E Markowitz15. 1. Division of STD Prevention, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road, NE MS-E02, Atlanta, GA 30333, USA. Electronic address: shariri@cdc.gov. 2. Center for Community Health and Department of Medicine, University of Rochester School of Medicine and Dentistry, 46 Prince Street, Rochester, NY 14607, USA. Electronic address: nancy_bennett@urmc.rochester.edu. 3. Division of Epidemiology of Microbial Diseases, Yale School of Public Health, 60 College Street, P.O. Box 208034, New Haven, CT 06520, USA. Electronic address: linda.niccolai@yale.edu. 4. HIV/STD/TB Program, Center for Public Health Practice, Oregon Public Health Division, 800 NE Oregon Street, Suite 1130, Portland, OR 97232, USA. Electronic address: sean.schafer@state.or.us. 5. STD Control Branch, California Department of Public Health, 850 Marina Bay Parkway, Bldg P, 2nd Floor, Richmond, CA 94804, USA. Electronic address: ina.park@cdph.ca.gov. 6. Departments of Internal Medicine, Vanderbilt University Medical Center, A-2200 MCN, Nashville, TN 37232, USA. Electronic address: karen.bloch@vanderbilt.edu. 7. Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE MS-G41, Atlanta, GA 30333, USA. Electronic address: eunger@cdc.gov. 8. STD Control Branch, California Department of Public Health, 850 Marina Bay Parkway, Bldg P, 2nd Floor, Richmond, CA 94804, USA. Electronic address: erin.whitney@cdph.ca.gov. 9. Division of Epidemiology of Microbial Diseases, Yale School of Public Health, 60 College Street, P.O. Box 208034, New Haven, CT 06520, USA. Electronic address: pamela.julian@yale.edu. 10. Center for Community Health and Department of Medicine, University of Rochester School of Medicine and Dentistry, 46 Prince Street, Rochester, NY 14607, USA. Electronic address: maryw_scahill@urmc.rocheter.edu. 11. HIV/STD/TB Program, Center for Public Health Practice, Oregon Public Health Division, 800 NE Oregon Street, Suite 1130, Portland, OR 97232, USA. Electronic address: nasreen.abdullah@state.or.us. 12. Departments of Internal Medicine, Vanderbilt University Medical Center, A-2200 MCN, Nashville, TN 37232, USA. Electronic address: diane.levine@vanderbilt.edu. 13. Division of STD Prevention, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road, NE MS-E02, Atlanta, GA 30333, USA. Electronic address: huk3@cdc.gov. 14. Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE MS-G41, Atlanta, GA 30333, USA. Electronic address: msteinau@cdc.gov. 15. Division of STD Prevention, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road, NE MS-E02, Atlanta, GA 30333, USA. Electronic address: lmarkowitz@cdc.gov.
Abstract
BACKGROUND: Prevention of pre-invasive cervical lesions is an important benefit of HPV vaccines, but demonstrating impact on these lesions is impeded by changes in cervical cancer screening. Monitoring vaccine-types associated with lesions can help distinguish vaccine impact from screening effects. We examined trends in prevalence of HPV 16/18 types detected in cervical intraepithelial neoplasia 2, 3, and adenocarcinoma in situ (CIN2+) among women diagnosed with CIN2+ from 2008 to 2012 by vaccination status. We estimated vaccine effectiveness against HPV 16/18-attributable CIN2+ among women who received ≥1 dose by increasing time intervals between date of first vaccination and the screening test that led to detection of CIN2+ lesion. METHODS: Data are from a population-based sentinel surveillance system to monitor HPV vaccine impact on type-specific CIN2+ among adult female residents of five catchment areas in California, Connecticut, New York, Oregon, and Tennessee. Vaccination and cervical cancer screening information was retrieved. Archived diagnostic specimens were obtained from reporting laboratories for HPV DNA typing. RESULTS: From 2008 to 2012, prevalence of HPV 16/18 in CIN2+ lesions statistically significantly decreased from 53.6% to 28.4% among women who received at least one dose (Ptrend<.001) but not among unvaccinated women (57.1% vs 52.5%; Ptrend=.08) or women with unknown vaccination status (55.0% vs 50.5%; Ptrend=.71). Estimated vaccine effectiveness for prevention of HPV 16/18-attributable CIN2+ was 21% (95% CI: 1-37), 49% (95% CI: 28-64), and 72% (95% CI: 45-86) in women who initiated vaccination 25-36 months, 37-48 months, and >48 months prior to the screening test that led to CIN2+ diagnosis. CONCLUSIONS: Population-based data from the United States indicate significant reductions in CIN2+ lesions attributable to types targeted by the vaccines and increasing HPV vaccine effectiveness with increasing interval between first vaccination and earliest detection of cervical disease. Published by Elsevier Ltd.
BACKGROUND: Prevention of pre-invasive cervical lesions is an important benefit of HPV vaccines, but demonstrating impact on these lesions is impeded by changes in cervical cancer screening. Monitoring vaccine-types associated with lesions can help distinguish vaccine impact from screening effects. We examined trends in prevalence of HPV 16/18 types detected in cervical intraepithelial neoplasia 2, 3, and adenocarcinoma in situ (CIN2+) among women diagnosed with CIN2+ from 2008 to 2012 by vaccination status. We estimated vaccine effectiveness against HPV 16/18-attributable CIN2+ among women who received ≥1 dose by increasing time intervals between date of first vaccination and the screening test that led to detection of CIN2+ lesion. METHODS: Data are from a population-based sentinel surveillance system to monitor HPV vaccine impact on type-specific CIN2+ among adult female residents of five catchment areas in California, Connecticut, New York, Oregon, and Tennessee. Vaccination and cervical cancer screening information was retrieved. Archived diagnostic specimens were obtained from reporting laboratories for HPV DNA typing. RESULTS: From 2008 to 2012, prevalence of HPV 16/18 in CIN2+ lesions statistically significantly decreased from 53.6% to 28.4% among women who received at least one dose (Ptrend<.001) but not among unvaccinated women (57.1% vs 52.5%; Ptrend=.08) or women with unknown vaccination status (55.0% vs 50.5%; Ptrend=.71). Estimated vaccine effectiveness for prevention of HPV 16/18-attributable CIN2+ was 21% (95% CI: 1-37), 49% (95% CI: 28-64), and 72% (95% CI: 45-86) in women who initiated vaccination 25-36 months, 37-48 months, and >48 months prior to the screening test that led to CIN2+ diagnosis. CONCLUSIONS: Population-based data from the United States indicate significant reductions in CIN2+ lesions attributable to types targeted by the vaccines and increasing HPV vaccine effectiveness with increasing interval between first vaccination and earliest detection of cervical disease. Published by Elsevier Ltd.
Entities:
Keywords:
CIN; Cervical intraepithelial neoplasia; HPV; High grade cervical lesion; Human papillomavirus; Vaccine
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