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Impact of bivalent human papillomavirus (HPV) vaccination upon the risk of acquisition of other HPV types

Breanne E. Biondi, Stanley H. Weiss

Abstract


The first human papillomavirus (HPV) vaccine was approved by the FDA in 2006, protecting against 2 carcinogenic types, 16 and 18. There is limited information about whether that vaccination may affect the prevalence of other HPV types in a community over time. Our study aimed to examine this issue. We used published data from The Costa Rica Vaccine Trial. Women were vaccinated with either the Cervarix® HPV vaccine or the hepatitis A vaccine (the control group). Based upon laboratory data, each of these arms can be divided into a naïve cohort with no evidence of HPV infection on trial entry and the rest considered a non-naïve cohort with baseline infection with HPV.

At the end of a 4-year follow-up, women in the combined non-naïve cohort had higher rates of HPV (mean number of HPV types detected per woman = 1.22) compared to the combined naïve cohort (mean number of HPV types detected per woman = 0.917), consistent with their presumptive higher risk profile upon study entry.  However, there was considerable variation by HPV type. Comparing those vaccinated against HPV to the control group, those in the non-naïve cohort had an increased prevalence of HPV type 35 (RR=1.37, 95%CI [0.88, 2.11]), and significantly increased prevalence of HPV types 51 and 59 (RR=1.34 [1.03, 1.74] and 1.86 [1.15, 3.00]) respectively). This could be the result of increased HPV infection with these types after HPV 16/18 vaccination or HPV infection before trial entry.  Among the naïve cohort, there was decreased prevalence in the HPV vaccine arm of HPV type 31 (RR=0.30, 95% CI [.12, .79]) and type 45 (RR=0.18, 95% CI [0.02, 1.46]), suggesting possible cross protection to these HPV types.

The protective effects from the bivalent HPV vaccine in the non-naïve cohort further support the current public health practice of administering the HPV vaccine to young women, without regard to baseline HPV status.

On December 10, 2014, the FDA approved Gardasil 9®, which vaccinates for an additional 5 carcinogenic types of HPV (31, 33, 45, 52 and 58). The addition of these types to the HPV vaccine will be beneficial in decreasing infection with these HPV types, but our analysis looks at the possible implications of how this can affect acquisition types not featured in the vaccine. There was a high prevalence of HPV types 16, 51 and 52 among the total cohort. Types 51 and 52 are not in the prior HPV vaccines and type 51 is not in the new Gardasil 9® vaccine, so type 51 may continue at a high prevalence in some geographic areas and may pose especial risk in the coming years. The prevalences of the various HPV types differ, sometimes substantially, by region. Therefore, further studies examining the prevalence of HPV types over time by geography will be critical for providing guidance to vaccine manufacturers, as well as screening guidelines for clinicians.


Keywords


HPV; Vaccines; Cross-protection; Costa Rica; Epidemiology; human papillomavirus; Prevention; Public health; Infectious diseases; Viruses; screening; HPV types; HPV DNA; serology

References


Reference List

U.S. Food and Drug Administration. FDA approves Gardasil 9 for prevention of certain cancers caused by five additional types of HPV on December 10, 2014. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm426485.htm (Accessed December 18, 2014.)

Rodríguez AC, Solomon D, Herrero R et al. Impact of human papillomavirus vaccination on cervical cytology screening, colposcopy, and treatment. Am J Epidemiol 2013;178(5):752-760.

Wheeler CM, Kjaer SK, Sigurdsson K et al. The impact of quadrivalent human papillomavirus (HPV; types 6, 11, 16, and 18) L1 virus-like particle vaccine on infection and disease due to oncogenic nonvaccine HPV types in sexually active women aged 16-26 years. J Infect Dis 2009;199(7):936-944.

Brown DR, Kjaer SK, Sigurdsson K et al. The impact of quadrivalent human papillomavirus (HPV; types 6, 11, 16, and 18) L1 virus-like particle vaccine on infection and disease due to oncogenic nonvaccine HPV types in generally HPV-naive women aged 16-26 years. J Infect Dis 2009;199(7):926-935.

Hildesheim A, Herrero R, Wacholder S et al. Effect of human papillomavirus 16/18 L1 viruslike particle vaccine among young women with preexisting infection: a randomized trial. JAMA 2007;298(7):743-753.

Bosch FX, Manos MM, Munoz N et al. Prevalence of human papillomavirus in cervical cancer: a worldwide perspective. J Natl Cancer Inst 1995;87(11):796-802.

Bosch FX, Burchell AN, Schiffman M et al. Epidemiology and natural history of human papillomavirus infections and type-specific implications in cervical neoplasia. Vaccine 2008;26 Suppl 10:K1-16.

Saslow D, Solomon D, Lawson HW et al. American Cancer Society, American Society for Colposcopy and Cervical Pathology, and American Society for Clinical Pathology screening guidelines for the prevention and early detection of cervical cancer. Am J Clin Pathol 2012;137(4):516-542.

Massad LS, Einstein MH, Huh WK et al. 2012 updated consensus guidelines for the management of abnormal cervical cancer screening tests and cancer precursors. Obstet Gynecol 2013;121(4):829-846.




DOI: http://dx.doi.org/10.18103/mra.v0i1.24

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