Risk factors inducing the persistence of high‐risk genital papillomaviruses in the normal cervix

Abstract

To evaluate the risk factors associated with persistence of human papillomaviruses (HPV) types 16, 18, and 33 in the normal cervix, a prospective study was carried out in Belgium of 323 women without cytological evidence of cervical intraepithelial neoplasia. Demographic and clinical data were obtained by interview, and HPV DNA was assayed in cervical-swab specimens using the Fast Multiplex Polymerase Chain Reaction-based screening and confirmatory tests. A multivariable linear regression model was constructed using four well-known risk factors: the use of an oral contraceptive which is either triphasic, or monophasic and containing ethynylestradiol in association with either norethysterone, or levonorgestrel, or lynestrenol, or gestoden, or estrogenic and containing estriol (P = 8 x 10(-5)), a positive history of genital herpes simplex virus (HSV) infection (P = 10(-4)), an age inferior or equal to 30 years (P = 0.012), and cigarette smoking (P = 0.020). Crude and adjusted relative risks were calculated for each HPV persistence predictor. The data and the results of the molecular biology of high-risk genital HPVs are consistent with the hypothesis that the use of an oral contraceptive containing simultaneously and continuously both a potent estrogen and a high activity progestative is necessary to enhance significantly HPV transcription. These observations are also consistent with the hypothesis that the oral contraceptives and HSV genital infection are responsible for HPV persistence in the normal cervix but not for HPV-induced cervical transformation.(ABSTRACT TRUNCATED AT 250 WORDS)

High risk human papillomavirus in oral squamous carcinoma: evidence of risk factors in a Venezuelan rural population. Preliminary report

“…It will also identify situations where the frequency of HPV infection is so high relative to the frequency of neoplasias as to make HPV testing irrelevant. However, it has been shown that not all the HPV infections progress to oral cancer and that some of the precancerous lesions regress spontaneously (5). Therefore, some additional factors, environmental or endogenous, must modulate the evolution of HPV in the oral tissue.…”

Contraceptive use and reproductive history in women with cervical human papillomavirus infection

“…Nine found no correlation between CHPI and OC use [4,7,[8][9][10][22][23][24][25], although the odds ratios were more than 1.0 in most studies. In five studies [5, [26][27][28][29], the OC use was significantly correlated with CHPI. One of these studies [5] adjusted for number of lifetime sexual partners but no other sexual risk behavior factors.…”

“…One of these studies [5] adjusted for number of lifetime sexual partners but no other sexual risk behavior factors. One study [27] addressed the problem of OC type between monophasic and triphasic OCs, but did not stratify into different potencies. Three previous studies [5,9,23] have included data on duration of OC use.…”

A matched prospective study of human immunodeficiency virus serostatus, human papillomavirus DNA, and cervical lesions detected by cytology and colposcopy

“…Although other cervical infections have been suggested as cofactors for activation of latent HPV in the cervix, 23 larger trials where multivariate analyses are possible would be needed to test for potential independent cofactors in HPV DNA expression.…”