The epidemiology of genital human papillomavirus infection
Introduction
More than 120 different human papillomavirus (HPV) types have been catalogued so far [1], [2], of which more than 40 infect the epithelial lining of the anogenital tract and other mucosal areas of the body. Some 13–18 types have been identified as probable or definite high-oncogenic risk HPV types (HR-HPV) (Table 1). It is now widely accepted that HR-HPV infections are a necessary, but not sufficient, cause of virtually all cases of cervical cancer worldwide and are a likely cause of a substantial proportion of other anogenital neoplasms and oral squamous cell carcinomas. Infection with low oncogenic risk HPV types (LR-HPV), such as HPV 6 and 11, can cause benign lesions of the anogenital areas known as condylomata acuminata (genital warts), as well as a large proportion of low-grade squamous intraepithelial lesions of the cervix. LR-HPV clinical infections are responsible for substantial morbidity and invoke high costs associated with the treatment of clinically relevant lesions. In this report, we review the essential aspects of the epidemiology of genital HPV infections and outline the risk factors for becoming infected with an emphasis on the role of HPVs as cancer causing agents, particularly cervical carcinomas.
Section snippets
How common is genital HPV infection?
HPV infections are the most common diagnosed sexually transmitted diseases today. Studies utilizing HPV DNA testing of asymptomatic women in the general population estimate the prevalence of HPV infection to be in the range of 2–44% [3], [4], [5], [6], [7], [8], [9]. This wide variation in prevalence estimates is largely explained by age differences among population samples studied, and by differences in the molecular sensitivity of the various HPV DNA assays used to detect viral DNA [7]. It is
HPV infection as the causal intermediate in cervical carcinogenesis
Fig. 2 shows the various components of the etiological model for the natural history of HPV infection and cervical carcinogenesis. The distal risk factor is sexual activity, which has been known for at least five decades to be the most important correlate of cervical cancer risk. As discussed above, the role of persistent HPV infection is central to this etiologic model.
A role for HPV infection in the sexually transmitted disease model of cervical cancer was proposed in the mid-1970s [57].
Risk factors for HPV infection
Risk determinants for HPV infection that have been identified in various cross-sectional and prospective cohort studies include number of sexual partners (lifetime and recent), age at first intercourse, smoking, oral contraceptive (OC) use, other STIs (e.g. chlamydia and herpes simplex virus), chronic inflammation, immunosuppressive conditions including HIV infection, and parity [8], [31], [47], [67], [68], [69], [70]. Results have been inconsistent partly owing to the fact that different
Conclusion
Molecular epidemiologic studies of the natural history of HPV infection and cervical neoplasia have provided much of the knowledge base that has led to the ongoing paradigm changes in cervical cancer prevention via HPV screening and HPV vaccination. The contributions of epidemiology in this process during the last 15 years have been focused on the demonstration that HPV infection is the cause of cervical cancer, and as such, they have dealt with the virus mostly as an intermediate endpoint in
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