**1. Introduction**

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Diagnostic methods for the detection of HPV should increase standardization and reproduci‐ bility due to two significant events in the future: the epidemiological monitoring changes in a vaccinated population and the involvement of HPV in tumors of other anatomical sites.

It will be necessary to diagnose HPV in processes other than cervical cancer, and we refer not only to their involvement in tumors with a demonstrated relationship, as in the anal region, but also to other locations in which their participation is suggested, as in the oropharyngeal tumors. Standardization in the collection and sample processing will be crucial in order to achieve accurate results involving an aid in the diagnosis and prognosis of these processes and their possible prevention.

However, the future challenge will be presented with the changes caused by the vaccination campaigns and their influence on the prevalence of cytological abnormalities and screening programs that will need to be designed according to the new status. There are already published results showing a decrease in the incidence of HPV in young women vaccinated Australia and confirm the estimates of predictive models [1].

Vaccination impact monitoring requires a multidisciplinary collaboration with technical and information support adequate to provide significant evidence to justify changes in health measures. However, screening should remain as an important strategy in cervical cancer control in both vaccinated and unvaccinated people. The reduction in incidence in young women after mass vaccination of adolescents together with greater range in controls and improved sensitivity of HPV testing draws a picture with attractive screening programs more efficient and cost effective in disease control.

properly cited.

© 2013 Galán-Sánchez and Rodríguez-Iglesias; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The availability of sensitive diagnostic assays for HPV, reproducible and cost effectively will be critical in the monitoring of current vaccines and the design and implementation of vaccination programs. The HPV vaccine offers a unique opportunity to fight against cancer and diseases associated with HPV infection.

state. However, animal models of papillomavirus infection have provided sufficient experi‐ mental evidence for papillomavirus latency [8]. HPV infects basal epithelial cells at sites of microtrauma, likely a normal consequence of sexual intercourse. Infected basal cells induced to differentiate to fill the wound will result in active papillomavirus infection. A few infected basal stem cells will retain HPV, but do not differentiate, and these infected cells are unlikely to be sampled using standard exfoliative techniques employed in most epidemiologic studies, which sample only the surface epithelium. Thus, HPV in a basal stem cell may remain undetectable until triggered to differentiate by undetermined stimuli such as wound repair and hormonal regulation [9]. With high cellular turnover in the cervical epithelium, one may expect relatively constant detection of HPV in this model. However, it is likely that a reacti‐ vated infection subsequent to latently infected stem cell differentiation is immediately recognized and brought under control by a functional memory immune response resulting in very short duration of active infection. This model would be consistent with the increase in new HPV DNA detection immediately following memory T cell depletion in acute HIV and in sexually abstinent women with chronic HIV infection [10, 11]. The relatively lower rates of recurrent HPV DNA detection in healthy populations suggests that the normal immune response is able to retain recurrence, but that background reactivation is common and likely

HPV Diagnosis in Vaccination Era http://dx.doi.org/10.5772/55818 59

Among sexually active males, genital HPV infection is also very common; however, prevalence varies widely depending on geographic region, risk group, anatomical site, sampling method, and HPV testing methodology [13, 14]. In a recent systematic review, Smith et al [15] estimated HPV prevalence to be between 1% and 84% in low-risk sexually active men, and between 2% and 93% in high risk men. HPV infection declines substantially after about 30 years of age, The prevalence of HPV infection in males generally remains constant or declines only slightly with age after peak prevalence. One possible explanation for this is that men experience a higher rate of reinfection compared to women. Anal cancer is very rare in the general population, but much more common in well defined, high-risk populations, including women with a previous cervical precancer, men having sex with men (MSM), and immune-compromised individuals. Infection with carcinogenic human papillomavirus (HPV) has been increasingly recognised to cause anal cancer and Machalek et al [16] recorded a prevalence of high-risk anal HPV in HIV-

In 1995, the International Agency for Research on Cancer (IARC) first classified HPV types 16 and 18 as carcinogenic to humans, but based on more recent evidence, the list of carcinogenic HPV types has been expanded to include a total of 13 mucosotropic anogenital HPV types as being definite or probable carcinogens (grade 1 or 2a) based on their frequent association with invasive cervical cancer (ICC) and cervical intraepithelial neoplasia (CIN) [17]. The oncogenic types (mostly HPV 16) are also causally implicated in other cancers, including penile, anal, vulvar and vaginal cancers [18, 19]. The remaining genital types (e.g., HPV types 6, 11, 42, 43, 44 and some rarer types) are considered to be of low or no oncogenic risk [20]. However, these types may cause subclinical and clinically visible benign lesions known as flat and acuminate

associated with short duration of detectable viral DNA [12].

positive MSM of 73.5%.

condylomata, respectively.
