2Epidemiology and burden of HPV-related disease
Introduction
Although most human papillomavirus (HPV) infections do not cause symptoms and resolve spontaneously, persistent infection with oncogenic HPV types, also known as high-risk (HR) HPVs, may lead to precancerous lesions and cancer. HR HPVs are not only responsible for virtually all cervical cancer cases, but are also causally related with a variable fraction of other anogenital cancers (vulvar, vaginal, penile, and anal cancers) and a subset of head and neck cancers, particularly base of tongue cancer, tonsil cancer, and other oropharyngeal cancer sites [1], [2], [3].
Among the more than 200 genotypes of HPVs identified to date, only a few are responsible for most of the burden of disease. The last International Agency for Research on Cancer (IARC) classification defined 12 HPV types as carcinogenic to humans, namely HPVs 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, and 59 (Group 1) [4]. Within them, HPV16 and HPV18 stand out for their highest carcinogenic capacity [5].
In the last decade, cervical cancer screening based on HPV testing and prophylactic HPV vaccination have radically changed the perspective of diagnosis and prevention of cervical neoplasia and the rest of HPV-related diseases. However, HPV infection remains one of the major causes of infection-related cancer in both men and women, particularly in less developed countries [6].
The aim of this paper is therefore to provide an overview of the global prevalence of HPV infection and HPV-related disease by geographical region and cancer site. Special emphasis is given to cervical cancer as it accounts for more than 80% of cancers attributable to HPV infection [7]. Consideration is also given to genital warts, a major cause of morbidity worldwide, caused mainly by low-risk (LR) HPV6 and HPV11.
Section snippets
HPV infection in women with normal cytological findings
The most updated data estimating HPV infection among women with normal cervical cytology is based on systematic reviews and meta-analysis performed by the Institut Català d’Oncologia (ICO)/IARC Information Centre on HPV and Cancer [8], ∗[9]. The global prevalence of HPV infection is estimated as 11.7% (95% confidence interval: 11.6–11.7), although there are considerable regional differences and substantial variations from study to study. Particularly high prevalence of HPV infection is seen in
Burden of cancers attributable to HPV infection
In 2012, approximately 4.5% (640,000 cases) of new cancer cases were attributable to HPV infection. HPV represented 29.5% of infection-related cancers worldwide in 2012 and caused more than half of all infection-attributable cancers in women (570,000 cases), in which cervical cancer accounts for more than 80% of cases ∗[6], ∗[7], [16].
Conclusions
Continuous monitoring and quantification of cancer burden is critical for cancer control. Differences in cervical cancer burden among populations are mainly the result of historical disparities on cervical cancer prevention.
Cervical cancer has been effectively controlled by cytological screening and treatment in many high-income countries, while they are not feasible at scale in low-resource settings. The elevated rates of cervical cancer reported in less developed regions result from poor
Summary
Overall, 630,000 cancer cases (4.5% of all cancer cases) are attributable to HPV every year, representing a major threat to public health worldwide. HPV-related cancers account for 8.6% (570,000 cases) of all cancer cases in women and 0.8% (60,000 cases) of all cancer cases in men and caused more than half of all infection-attributable cancers in women in 2012. The vast majority (83.0%) of cancer cases attributable to HPV are cervical cancer cases (528,000 cases), followed by head and neck
Conflict of interest
Authors declare no competing interests. The Unit of Infections and Cancer has received unrestricted research grants from GlaxoSmithKline, Merck, and Sanofi Pasteur MSD. Xavier F. Bosch has acted as a consultant for Merck and receives honorarium for lectures or travel support from Merck, Qiagen, Roche, Sanofi Pasteur MSD, and GlaxoSmithKline.
Acknowledgments
This work was partially supported by grants from the Instituto de Salud Carlos III-ISCII (Spanish Government) co-funded by FEDER funds/European Regional Development Fund (ERDF) – A WAY TO BUILD Europe (References: Redes temáticas de investigación cooperative en salud (RETICS) RD12/0036/0056, Centro de Investigación Médica en Red Ciber-Cancer: CB16/12/00401), Agencia de Gestión de Ayudas Universitarias y de Investigación (AGAUR) de la Generalitat de Catalunya (2014SGR1077) and Recercaixa 2015 (
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