Oral Human Papillomavirus Infection in Children during the First 6 Years of Life, Finland.

Human papillomavirus (HPV) infections are found in children, but transmission modes and outcomes are incompletely understood. We evaluated oral samples from 331 children in Finland who participated in the Finnish Family HPV Study from birth during 9 follow-up visits (mean time 51.9 months). We tested samples for 24 HPV genotypes. Oral HPV prevalence for children varied from 8.7% (at a 36-month visit) to 22.8% (at birth), and 18 HPV genotypes were identified. HPV16 was the most prevalent type to persist, followed by HPV18, HPV33, and HPV6. Persistent, oral, high-risk HPV infection for children was associated with oral HPV carriage of the mother at birth and seroconversion of the mother to high-risk HPV during follow-up (odds ratio 1.60-1.92, 95% CI 1.02-2.74). Children acquire their first oral HPV infection at an early age. The HPV status of the mother has a major impact on the outcome of oral HPV persistence for her offspring.

Breast Milk Is a Potential Vehicle for Human Papillomavirus Transmission to Oral Mucosa of the Spouse.

BACKGROUND: Human papillomavirus (HPV) DNA has been detected in breast milk, but its origin has remained obscure. The aim of the study was to analyze the prevalence and persistence of HPV in breast milk in the Finnish Family HPV cohort study. The association of breast milk HPV positivity with the family members' oral HPV status was evaluated. METHODS: We included 308 families to the study where the mother was breast feeding her offspring. Mothers collected the milk samples manually at day 3, and at months 2, 6 and 12. Cervical and/or oral samples were collected from all family members. HPV testing was performed using nested polymerase chain reaction and Luminex-based Multimetrix kit. RESULTS: Breast milk HPV DNA was found in 10.1% (31/308), 20.1% (39/194) and 28.8% (17/59) of samples at day 3, months 2 and 6, respectively. The following HPV genotypes were detected: 6, 16, 18, 33, 45, 53, 56, 59, 66 and 82. Breast milk HPV persisted among 5.5% (9/164) of the lactating mothers. No significant associations were detected between the persistent breast milk HPV and the offspring's oral incident HPV infection. Breast milk HPV positivity showed a strong association with the fathers' oral HPV positivity at baseline, as well as at 6- and 12-month follow-up visits, with odds ratio (OR) = 3.24 [95% confidence interval (CI): 1.04-10.12], OR = 6.34 (95% CI: 1.84-21.89) and OR = 14.25 (95% CI: 1.16-174.80), respectively. CONCLUSIONS: HPV in breast milk is prevalent among the lactating mothers and HPV can also persist in breast milk. The breast milk is a potential vehicle for HPV transmission to oral mucosa of the spouse but not of the offspring.

Dynamics of human papillomavirus serology in women followed up for 36 months after pregnancy.

We determined L1 antibodies for human papillomavirus (HPV) types 6, 11, 16, 18 and 45 by multiplex serology in our prospective HPV family study. We report seroprevalence, seroconversion and antibody decay in 290 women (mean age, 25.5 years) sampled before delivery and at 12, 24 and 36 months of follow-up. Multiplex HPV genotyping of the baseline oral and genital scrapings was performed. At baseline, seroprevalence of HPV 6, 11, 16, 18 and 45 was 53.3, 21.5, 34.9, 21.5 and 9.0%, respectively. Seropositivity for low-risk HPV (LR-HPV) was associated significantly with age at onset of sexual activity (P=0.001), number of sexual partners until age 20 (P=0.018), lifetime number of sexual partners (P=0.0001), history of genital warts (P=0.0001) and being seropositive for high-risk (HR) HPV (P=0.0001). The same covariates also predicted seropositivity for HR-HPV. During follow-up, 26.7, 13.9, 17.0, 16.8 and 6.6% of the women seroconverted to L1 antigen of HPV 6, 11, 16, 18 and 45, respectively, between 18.2 and 23.8 months. Independent predictors of seroconversion to LR-HPV were unemployment (P=0.019) and absence of anal sex practice (P=0.031), and to HR-HPV, absence of smoking history and lifetime number of sexual partners. Decay of HPV 6, 11, 16, 18 and 45 antibodies was observed in 2.3, 4.0, 5.3, 4.5 and 1.5 % of the women, respectively, with decay time varying from 27.2 to 35.8 months. These data imply that (i) a substantial proportion of young women are seropositive for both LR- and HR-HPV types, (ii) they frequently undergo seroconversion within 18-24 months, predicted by common covariates, and (iii) antibody decay over 3 years is rare.

Effect of second pregnancy on maternal carriage and outcome of high-risk human papillomavirus (HPV). Experience from the prospective finnish family HPV study.

OBJECTIVES: The effect of second pregnancy on human papillomavirus (HPV) carriage and outcome is modelled in longitudinal setting covering two subsequent pregnancies. STUDY DESIGN: Among 329 (baseline pregnant) women prospectively followed up in the Finnish Family HPV Study, two subcohorts were compiled: (i) 78 women (Group B) who became pregnant for the second time during the follow-up, and (ii) 100 women (Group A) who did not develop 2nd pregnancy. The effect of pregnancy on high-risk HPV (HR-HPV) carriage and outcome was analysed using Kaplan-Meier and Cox survival analyses and generalized estimating equation (GEE) modelling of the longitudinal data. RESULTS: Women in the two groups were similar in their baseline HR-HPV status but significantly different in several known risk factors of HR-HPV infection. Group A women showed higher point prevalence of cervical and oral HR-HPV at the 36-month (p = 0.015) and 6-month (p = 0.024) follow-up visit, respectively. Among Group B women, prevalence of both cervical and oral HR-HPV significantly decreased during 2nd pregnancy (p = 0.005 and p = 0.002) as compared with inter-pregnancy period, but increased again after 2nd pregnancy. There was no difference in acquisition or clearance of cervical or oral HR-HPV between the two groups in univariate (Kaplan-Meier) or multivariate (Cox) survival analysis. In the GEE approach, 2nd pregnancy was not significantly associated with cervical or oral HR-HPV carriage or persistence when adjusted for all other covariates. CONCLUSIONS: Second pregnancy is of little impact on carriage and persistence of oral and cervical HR-HPV infections in a longitudinal setting over time.

Human papillomavirus in the placenta and umbilical cord blood.

OBJECTIVE: To analyze human papillomavirus (HPV) DNA in umbilical cord blood and in placenta, including its cellular localization. DESIGN: Longitudinal prospective study. SETTING: Maternity Unit of Turku University Hospital, and MediCity, University of Turku. SAMPLES: Placental and cord blood samples obtained at delivery from 315 mothers and 311 neonates included in the Finnish HPV Family Study. METHODS: HPV testing by nested PCR and sequencing. Tyramide amplified in situ hybridization (ISH) for viral DNA localization in placenta. Correlation to mother's and neonate's oral and genital HPV status and maternal demographic data. MAIN OUTCOME MEASURES: Detection and cellular localization of HPV DNA. RESULTS: HPV DNA was detected in 4.2 and 3.5% of placenta and cord blood samples, respectively, including HPV types 16, 6, 83 and 39. In placenta, HPV6 and 16 DNA was localized in syncytiotrophoblasts. Abnormal cytology increased the risk of HPV+ placenta and cord blood. History of genital warts was the only independent predictor of cord blood HPV in multivariate analysis (adjusted OR=4.0, 95% CI: 1.09-14.54, p=0.036). HPV DNA in cord blood increased the risk of genital (OR=4.0, 95% CI: 1.08-14.83, p=0.048) and oral (OR=4.4, 95% CI: 1.17-16.14, p=0.039) HPV DNA carriage of the neonate. HPV+ placenta increased the risk of oral HPV of the neonate (OR=8.6, 95% CI: 2.73-27.13, p=0.0001). Delivery mode did not predict HPV status of the neonate. CONCLUSIONS: HPV DNA is detected in placental trophoblasts and umbilical cord blood. The presence of HPV DNA at these sites increases the risk of a neonate testing HPV-positive at birth.

Human papillomavirus DNA detected in breast milk.

Human papillomavirus (HPV) testing of 223 breast milk samples 3 days postpartum was performed with polymerase chain reaction, hybridization, and sequencing. HPV-16-DNA was detected in 4.0% of the samples. HPV carriage in the breast milk was not correlated with mother's oral or cervical HPV-status or the demographic data. Oral HPV-infection of the spouse at month 6 and 12 postpartum was statistically significantly associated with HPV carriage in the breast milk.