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dc.contributor.authorTrottier, Helen
dc.contributor.authorFranco, Eduardo L.
dc.date.accessioned2009-05-25T07:47:12Z
dc.date.available2009-05-25T07:47:12Z
dc.date.issued2006-03-30
dc.identifier.citationVaccine 2006, 24 Suppl 1:S1-15en
dc.identifier.issn0264-410X
dc.identifier.pmid16406226
dc.identifier.doi10.1016/j.vaccine.2005.09.054
dc.identifier.urihttp://hdl.handle.net/10146/68854
dc.descriptionKEYWORDS - CLASSIFICATION: cancer epidemiology;complications;Canada;epidemiology;Evaluation;Female;Genital Diseases,Female;Humans;Incidence;lifestyle modulation of cancer & cancer biomarkers;Papillomaviridae;Papillomavirus Infections;Risk Factors;Uterine Cervical Neoplasms;virology.en
dc.description.abstractClinical and subclinical human papillomavirus (HPV) infections are the most common sexually transmitted infections in the world, and most sexually-active individuals are likely to be exposed to HPV infection during their lifetimes. More than 40 genotypes of HPV infect the epithelial lining of the anogenital tract and other mucosal areas of the body; of these, 13-18 types are considered to be high-oncogenic risk HPV types (HR-HPV). Persistent infection with HR-HPVs is now unequivocally established as a necessary cause of cervical cancer and is likely to be responsible for a substantial proportion of other anogenital neoplasms and upper aero-digestive tract cancers. Low oncogenic risk HPV types (LR-HPV) are also responsible for considerable morbidity as the cause of genital warts. Youth and certain sexual characteristics are key risk factors for HPV acquisition and persistence of HPV infection, but other mediating factors include smoking, oral contraceptive (OC) use, other STIs (e.g. chlamydia, herpes simplex virus), chronic inflammation, immunosuppressive conditions including HIV infection, parity, dietary factors, and polymorphisms in the human leukocyte antigen system. Not surprisingly, these factors are also established or candidate cofactors identified in epidemiologic studies of cervical cancer. HPV transmissibility and molecular events in HPV-induced carcinogenesis have been the focus of recent multidisciplinary epidemiologic studies. This shift in research focus coincides with a shift in cancer prevention techniques towards immunization with HPV vaccines and HPV testing of precancerous lesions.
dc.language.isoenen
dc.relation.urlhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TD4-4HSXV6N-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=e0844e868560c684c5f91c05bc0519a5en
dc.subjectGenital human papillomavirusen
dc.subjectEpidemiologyen
dc.subjectCervical canceren
dc.subject.meshFemale
dc.subject.meshGenital Diseases, Female
dc.subject.meshHumans
dc.subject.meshIncidence
dc.subject.meshPapillomaviridae
dc.subject.meshPapillomavirus Infections
dc.subject.meshRisk Factors
dc.subject.meshUterine Cervical Neoplasms
dc.titleThe epidemiology of genital human papillomavirus infection.en
dc.typeArticleen
dc.identifier.journalVaccineen
html.description.abstractClinical and subclinical human papillomavirus (HPV) infections are the most common sexually transmitted infections in the world, and most sexually-active individuals are likely to be exposed to HPV infection during their lifetimes. More than 40 genotypes of HPV infect the epithelial lining of the anogenital tract and other mucosal areas of the body; of these, 13-18 types are considered to be high-oncogenic risk HPV types (HR-HPV). Persistent infection with HR-HPVs is now unequivocally established as a necessary cause of cervical cancer and is likely to be responsible for a substantial proportion of other anogenital neoplasms and upper aero-digestive tract cancers. Low oncogenic risk HPV types (LR-HPV) are also responsible for considerable morbidity as the cause of genital warts. Youth and certain sexual characteristics are key risk factors for HPV acquisition and persistence of HPV infection, but other mediating factors include smoking, oral contraceptive (OC) use, other STIs (e.g. chlamydia, herpes simplex virus), chronic inflammation, immunosuppressive conditions including HIV infection, parity, dietary factors, and polymorphisms in the human leukocyte antigen system. Not surprisingly, these factors are also established or candidate cofactors identified in epidemiologic studies of cervical cancer. HPV transmissibility and molecular events in HPV-induced carcinogenesis have been the focus of recent multidisciplinary epidemiologic studies. This shift in research focus coincides with a shift in cancer prevention techniques towards immunization with HPV vaccines and HPV testing of precancerous lesions.


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