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      Human papillomavirus (HPV) perinatal transmission and risk of HPV persistence among children: Design, methods and preliminary results of the HERITAGE study

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          Abstract

          Perinatal route of transmission of human papillomavirus (HPV) has been demonstrated in several small studies. We designed a large prospective cohort study (HERITAGE) to better understand perinatal HPV. The objective of this article is to present the study design and preliminary data. In the first phase of the study, we recruited 167 women in Montreal, Canada, during the first trimester of pregnancy. An additional 850 are currently being recruited in the ongoing phase. Cervicovaginal samples were obtained from mothers in the first trimester and tested for HPV DNA from 36 mucosal genotypes (and repeated in the third trimester for HPV-positive mothers). Placental samples were also taken for HPV DNA testing. Conjunctival, oral, pharyngeal and genital samples were collected for HPV DNA testing in children of HPV-positive mothers at every 3–6 months from birth until 2 years of age. Blood samples were collected in mother and children for HPV serology testing. We found a high prevalence of HPV in pregnant women (45%[95%CI:37–53%]) and in placentas (14%[8–21%]). The proportion of HPV positivity (any site) among children at birth/3-months was 11%[5–22%]. HPV was detected in children in multiple sites including the conjunctiva (5%[10–14%]). The ongoing HERITAGE cohort will help provide a better understanding of perinatal HPV.

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          Chapter 2: The burden of HPV-related cancers.

          On the basis of current evidence regarding human papillomavirus (HPV) and cancer, this chapter provides estimates of the global burden of HPV-related cancers, and the proportion that are actually "caused" by infection with HPV types, and therefore potentially preventable. We also present trends in incidence and mortality of these cancers in the past, and consider their likely future evolution.
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            Chapter 1: HPV in the etiology of human cancer.

            The causal role of human papillomavirus (HPV) in all cancers of the uterine cervix has been firmly established biologically and epidemiologically. Most cancers of the vagina and anus are likewise caused by HPV, as are a fraction of cancers of the vulva, penis, and oropharynx. HPV-16 and -18 account for about 70% of cancers of the cervix, vagina, and anus and for about 30-40% of cancers of the vulva, penis, and oropharynx. Other cancers causally linked to HPV are non-melanoma skin cancer and cancer of the conjunctiva. Although HPV is a necessary cause of cervical cancer, it is not a sufficient cause. Thus, other cofactors are necessary for progression from cervical HPV infection to cancer. Long-term use of hormonal contraceptives, high parity, tobacco smoking, and co-infection with HIV have been identified as established cofactors; co-infection with Chlamydia trachomatis (CT) and herpes simplex virus type-2 (HSV-2), immunosuppression, and certain dietary deficiencies are other probable cofactors. Genetic and immunological host factors and viral factors other than type, such as variants of type, viral load and viral integration, are likely to be important but have not been clearly identified.
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              The epidemiology of genital human papillomavirus infection.

              Clinical 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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                Author and article information

                Contributors
                Journal
                Papillomavirus Res
                Papillomavirus Res
                Papillomavirus Research
                Elsevier
                2405-8521
                12 July 2016
                December 2016
                12 July 2016
                : 2
                : 145-152
                Affiliations
                [a ]Department of Social and Preventive Medicine, Université de Montréal, Sainte-Justine Hospital, Montreal, Canada
                [b ]Departments of Obstetrics and Gynecology and Department of Social and Preventive Medicine, Université de Montréal and CRCHUM, Montreal, Canada
                [c ]Department of Microbiology, Université de Montréal and CRCHUM, Montreal, Canada
                [d ]Department of Obstetrics and Gynecology and the Research Institute of the McGill University Health Centre (RI-MUHC), McGill University, Royal Victoria Hospital, Montreal, Canada
                [e ]Sainte-Justine Hospital Research Center, Montreal, Canada
                [f ]Department of Pediatrics, Université de Montréal, Sainte-Justine Hospital, Montreal, Canada
                [g ]Department of Obstetrics and Gynecology, Université de Sherbrooke, Centre de recherche du CHUS, Canada
                [h ]Division of Clinical Epidemiology, McGill University Health Center, Montreal, Canada
                [i ]Department of Pediatrics, Division of Pediatric Intensive Care Medicine, Sainte-Justine Hospital, Université de Montréal, Canada
                [j ]Department of Obstetrics and Gynecology, Sainte-Justine Hospital, Montreal, Canada
                [k ]Department of Obstetrics and Gynecology, Centre Hospitalier de l′Université de Montréal (CHUM), Montreal, Canada
                [l ]Department of Obstetrics and Gynecology, St-Mary's Hospital Center, Montreal, Canada
                Author notes
                [* ]Correspondence to: Sainte-Justine Hospital Research Centre, Department of Social and Preventive Medicine, Université de Montréal, 3175 Côte Sainte-Catherine, Room A-830, Montreal, QC, Canada H3T 1C5.Sainte-Justine Hospital Research Centre, Department of Social and Preventive Medicine, Université de Montréal3175 Côte Sainte-Catherine, Room A-830MontrealQCH3T 1C5Canada helen.trottier@ 123456umontreal.ca
                Article
                S2405-8521(16)30026-X
                10.1016/j.pvr.2016.07.001
                5886899
                29074173
                bf749c0b-f45a-4d9c-aed9-5114716f0799
                © 2016 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 26 April 2016
                : 4 July 2016
                : 10 July 2016
                Categories
                Article

                human papillomavirus (hpv),perinatal transmission,pregnancy,placenta,children,persistence

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