Diagnosis and management of oncogenic cervical human papillomavirus infection

Document Type

Journal Article

Publication Date



Infectious Disease Clinics of North America








Cervical HPV infection should be managed less as a typical STI and more as a strong risk factor predisposing to cervical cancer development. HPV infection is undeniably transmitted predominately through sexual contact. However, the fact that more than 80% of women followed over time will acquire at least one HR-HPV infection reflects the ubiquitous nature of the infection and the ease of transmission. Although the behavioral profiles typically associated with an increased risk for STI (including lifetime partner number, age at first intercourse, and so forth) will certainly lead to an increased risk for HPV detection, there is a high absolute prevalence of HPV even among women who have few lifetime sex partners. It could be argued that to counsel patients for an HPV infection as an STI would be counterproductive, as short of absolute abstinence, the prevention of infection is difficult and treatment options, short of excisional procedures for neoplasia, are limited. The real promise held in this area is the availability of an apparently highly effective prophylactic HPV vaccine, targeting at least HPV 16, 18, 6, and 11 [33,34]. This vaccine cocktail, if it achieved 100% coverage, could theoretically prevent 50% to 70% of invasive cervical cancers and most genital warts. Vaccination will be required among women before initiation of sexual contact, presumably among girls 10 to 13 years of age. Many programmatic issues remain regarding the implementation of HPV vaccine programs, including the marketing of the vaccine as STI or cancer prevention, as reviewed in detail by Gravitt and Shah [72]. Even in the era of potentially effective vaccines, screening for cervical cancer is likely to remain a priority in cervical cancer prevention programs for at least several decades. Vaccine trials have proven high short-term efficacy; however, these effects were clearly type-specific and antibody titers gradually decrease postvaccination. It is unclear whether the protection will remain over an individual's lifetime without vaccine booster, and oncogenic HPV infections not targeted by vaccination will continue to contribute to risk for development of cervical intraepithelial neoplasia and cancer. Therefore, although the public health success of HPV vaccination is undoubtedly promising, the role of cervical cancer screening as a secondary prevention effort should not be trivialized. In fact, the nature of screening programs should continue to be reevaluated in the context of effective but limited spectrum vaccines. © 2005 Elsevier Inc. All rights reserved.