title: Age-related changes of the cervix influence human papillomavirus type distribution.
abstract: Approximately 15 human papillomavirus (HPV) types cause virtually all cervical cancer whereas other HPV types are unrelated to cancer. We were interested in whether some noncarcinogenic types differ from carcinogenic in their affinity for the cervical transformation zone, where nearly all HPV-induced cancers occur. To examine this possibility, we tested cervical specimens from 8,374 women without cervical precancer and cancer participating in a population-based study in Guanacaste for >40 HPV types using PCR. We compared age-group specific prevalences of HPV types of the alpha9 species, which are mainly carcinogenic and include HPV16, to the genetically distinct types of the alpha3/alpha15 species (e.g., HPV71), which are noncarcinogenic and common in vaginal specimens from hysterectomized women. We related HPV detection of each group to the location of the junction between the squamous epithelium of the ectocervix and vagina and the columnar epithelium of the endocervical canal. Models evaluated the independent effects of amount of exposed columnar epithelium (ectopy) and age on the presence of alpha9 or alpha3/alpha15 types. Prevalence of alpha9 types (7.6%) peaked in the youngest women, declined in middle-aged women, and then increased slightly in older women. By contrast, prevalence of alpha3/alpha15 types (7.6%) tended to remain invariant or to increase with increasing age. Detection of alpha9 infections increased (P(trend) < 0.0005) but alpha3/alpha15 infections decreased (P(trend) < 0.0005) with increasing exposure of the columnar epithelia. Older age and decreasing cervical ectopy were independently positively associated with having an alpha3/alpha15 infection compared with having an alpha9 infection. These patterns need to be confirmed in other studies and populations. We suggest that these genetically distinct groups of HPV types may differ in tissue preferences, which may contribute to their differences in carcinogenic potential.
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute/NIH, 6120 Executive Boulevard, Bethesda, MD 20892-7234, USA. castlep@mail.nih.gov
authors.forename: Philip E
authors.initials: PE
authors.lastname: Castle
authors.forename: Jose
authors.initials: J
authors.lastname: Jeronimo
authors.forename: Mark
authors.initials: M
authors.lastname: Schiffman
authors.forename: Rolando
authors.initials: R
authors.lastname: Herrero
authors.forename: Ana C
authors.initials: AC
authors.lastname: Rodríguez
authors.forename: M Concepción
authors.initials: MC
authors.lastname: Bratti
authors.forename: Allan
authors.initials: A
authors.lastname: Hildesheim
authors.forename: Sholom
authors.initials: S
authors.lastname: Wacholder
authors.forename: L Rodney
authors.initials: LR
authors.lastname: Long
authors.forename: Leif
authors.initials: L
authors.lastname: Neve
authors.forename: Ruth
authors.initials: R
authors.lastname: Pfeiffer
authors.forename: Robert D
authors.initials: RD
authors.lastname: Burk
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D002471:Cell Transformation, Neoplastic; D003364:Costa Rica / Q000453:epidemiology; D004279:DNA, Viral / Q000032:analysis; D016021:Epidemiologic Studies; D005260:Female; D006801:Humans; D007044:Hysterectomy; D008875:Middle Aged; D027383:Papillomaviridae / Q000235:genetics* / Q000472:pathogenicity*; D030361:Papillomavirus Infections / Q000150:complications* / Q000453:epidemiology*; D016133:Polymerase Chain Reaction; D011230:Precancerous Conditions; D015995:Prevalence; D002583:Uterine Cervical Neoplasms / Q000821:virology*; D014621:Vagina / Q000821:virology
chemical_list: D004279:DNA, Viral