Persistent human papillomavirus infection and cervical neoplasia (original) (raw)
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International Journal of Gynecology & Obstetrics, 2006
Cervical cancer has been recognized as a rare outcome of a common, sexually transmitted infection whose etiologic association is restricted to a few human papillomavirus (HPV) types. With optimal testing systems HPV DNA can be identified in nearly all specimens of invasive cervical cancer, and it is claimed that infection of the cervix with HPV is a necessary cause of cervical cancer. The evidence is consistent worldwide for squamous cell carcinomas (SCC), adenocarcinomas, and the vast majority (>95%) of the immediate cervical cancer precursors, namely high-grade squamous intraepithelial lesions (HSILs) ---also known as cervical intraepithelial neoplasia 3 (CIN 3) or carcinoma in situ. Cofactors that modify the risk for HPV DNA-positive women include the use of oral contraceptives (OCs) for 5 or more years, smoking, high parity (5 or more full-term pregnancies), and previous exposure to other sexually transmitted diseases such as Chlamydia trachomatis and herpes simplex virus type 2 (HSV-2). Women exposed to the human immunodeficiency virus (HIV) are at high risk for HPV infection, HPV DNA persistence, and progression of HPV lesions to cervical cancer.
Cofactors in human papillomavirus infection and cervical carcinogenesis
Archives of Gynecology and Obstetrics
Objective This study aimed to identify the effect of various risk factors as the promoters of HPV infection, and to identify which HPV-positive women may have an increased risk of developing cervical cancer. Methods Smear preparations were examined and classified according to the Bethesda system. HPV-DNA detection and genotyping was carried out using polymerase chain reaction combined with reverse hybridization line-probe assays. Age, smoking habit, age at first sexual intercourse, number of sexual partners, number of term births, contraceptive method, progesterone therapy, history of sexually transmitted diseases, history or existence of warts and existence of cervical infection were recorded. Results 642 women (96 women with abnormal cervical cytology and 546 women with normal cytology) provided cervical samples. Smoking habit, number of sexual partners, number of term births, history of sexually transmitted diseases, history or existence of warts and existence of cervical infection were identified as the promoters of HPV infection. History of sexually transmitted diseases, history or existence of warts and existence of cervical infection were identified as cofactors affecting progression from HPV infection to cervical cancer. Neither of contraceptive methods studied was related to HPV infection or coexistence with malign transformation to cervical cancer. Conclusion Information gathered from this study could be used to prioritize limited screening and treatment services to woman who have specific characteristics that may put them at an increased risk of HPV infection. Additionally, by identifying which women have a higher risk of cervical cancer; it may be possible to reduce the number of unnecessary colposcopies.
Human Papillomavirus and the Long-term Risk of Cervical Neoplasia
American Journal of Epidemiology, 2002
The risk of cervical neoplasia for women with normal Papanicolaou smears was calculated for those whose smears were human papillomavirus (HPV) positive and those whose smears were HPV negative. Data on 347 cases and controls were analyzed in a population-based, nested case-control study. Cases (n = 77) were women who participated in the Utrecht screening program (1976)(1977)(1978)(1979)(1980)(1981)(1982)(1983)(1984) in the Netherlands and who developed cervical intraepithelial neoplasia 3 or microinvasive or invasive squamous cervical cancer after having a negative smear (1980)(1981)(1982)(1983)(1984)(1985)(1986). Controls (n = 270) were matched on age (±5 years) and follow-up period. DNA was isolated from the Papanicolaou smears and was tested for the presence of HPV DNA by using the ultrasensitive broadspectrum, general short-fragment polymerase chain reaction. HPV was found in 55 (71%) of the baseline smears of the 77 cases and in 31 (11%) of those of the 270 controls. The age-adjusted odds ratios for developing cervical intraepithelial neoplasia or microinvasive or invasive cervical cancer were 19.2 (95 percent confidence interval (CI): 10.3, 35.7) for HPV positivity in general, 5.4 (95% CI: 1.5, 19.5) for infection with low-risk HPV genotypes, 24.0 (95% CI: 12.4, 46.4) for high-risk HPV genotypes, and 104.8 (95% CI: 29.5, 372.7) for HPV type 16. Am J
Journal of Clinical Virology, 2001
Background: Human papillomavirus (HPV) is the major cause of cervical neoplasia but estimates of the population attributable fraction (PAR%), of HPV vary. PAR% has not been derived from longitudinal studies although assessment of HPV exposure prior to the neoplasia diagnosis should increase validity of such estimates. Aims: Systematic review and meta-analysis of longitudinal studies on HPV associated relative risk (RR) for and PAR% of HPV16 in cervical neoplasia. Methods: Pertinent data from longitudinal studies was made available through Medline and substituted by various hand searches. HPV associated weighted mean RR, with 95% confidence interval (CI) of cervical neoplasia, and the PAR% of HPV16 in cervical carcinoma were estimated both for unselected and low HPV prevalence populations. Results: HPV associated RR of cervical carcinoma in PCR-based studies was 17 (95% CI 8.2-33). HPV16 associated RRs in seroepidemiological studies were 3.3 (95% CI 2.2-4.9) for the unselected population, HPV16 seroprevalence 11.0%, and 12.5 (95% CI 5.5-29) for a population with low HPV16 seroprevalence of 5.3%. Corresponding PAR% estimates of HPV16 were 27 and 44%, respectively. Conclusion: Protective vaccination against HPV16 infection would prevent up to 44% of cervical carcinoma.
Human Papillomavirus - Research in a Global Perspective, 2016
The prevalence of human papillomavirus (HPV) infection in males is comparable to females, although in men it is largely unknown. HPV infections may be connected with the development of carcinomas and other dermoepithelial changes such as intraepithelial neoplasia. Multidirectional studies have shown that chronic HPV infection is a necessary, though insufficient factor for the development of cervical cancer. Although men are regarded as the dominant vector of HPV transmission to their female sexual partners, they do not develop clinically significant HPV-related lesions and are usually asymptomatic during relatively short infections. Analysis of data from a multicenter, clinical preventive trial was to estimate the incidence of type-specific genital infection among men and HPV transmission dynamics. The routine clinical examination included a peniscopy and detection of HPV DNA in smears using hybrid capture and in biopsy material using PCR. It is necessary to establish prevention strategies for HPV infection in men whose female sexual partners have cervical cancer. Cervical cancer prevention strategies are likewise needed and should include the use of prophylactic HPV vaccines.
British Medical Journal, 2009
Objective To evaluate the cumulative incidence of cervical intraepithelial neoplasia II or worse (grade II+) or cervical intraepithelial neoplasia grade III+ after short term persistence of prevalently detected carcinogenic human papillomavirus (HPV). Design Population based cohort study. Setting Guanacaste, Costa Rica. Participants 2282 sexually active women actively followed after enrolment. Main outcome measures Primary end points: three year and five year cumulative incidence of histologically confirmed cervical intraepithelial neoplasia grade II+ (n=70). Cervical specimens collected at each visit tested for more than 40 HPV genotypes. HPV 16, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, 73, and 82 were considered the primary carcinogenic genotypes. Results Women who tested positive for a carcinogenic HPV at enrolment and after about one year (9-21 months) (positive/positive) had a three year cumulative incidence of cervical intraepithelial neoplasia grade II+ of 17.0% (95% confidence interval 12.1% to 22.0%). Those who tested negative/positive (3.4%, 0.1% to 6.8%), positive/ negative (1.2%, −0.2% to 2.5%), and negative/negative (0.5%, 0.1% to 0.9%) were at a significantly lower risk. There was little difference in the cumulative incidence of cervical intraepithelial neoplasia grade II+ between testing positive twice for any carcinogenic HPV genotype (same genotype or different genotypes) v testing positive twice for the same carcinogenic genotype (17.0% v 21.3%, respectively). Short term persistence of HPV 16 strongly predicted cervical intraepithelial neoplasia grade II+, with a three year cumulative incidence of 40.8% (26.4% to 55.1%). Similar patterns were observed for the five year cumulative incidence of grade II+ and for three year and five year cumulative incidence of grade III+. Conclusions Short term persistence of a prevalently detected carcinogenic HPV infection, especially HPV 16, strongly predicts a subsequent diagnosis of cervical intraepithelial neoplasia II+ over the next few years.