This study investigated the efficacy of the prophylactic human papillomavirus (HPV) vaccine, which was initiated between 2009 and 2013 in Japan. The study involved 1529 eligible women aged 16-39 years who visited 11 outpatient clinics in Japan for various reasons. These patients underwent HPV genotype analysis and a Pap test of cervical cell samples. A total of 299 women (19.6%) had received the prophylactic HPV vaccine (bivalent:quadrivalent vaccine ratio = 2:1). Of the 5062 participants in the Japanese Human Papillomavirus Disease Education and Research Survey (J-HERS 2011), which was conducted in the pre-vaccination era, 3236 eligible participants were included as controls. In this study (J-HERS 2021), the highest rate of HPV vaccination (53%) was observed in patients aged 22-27 years. Vaccinated individuals exhibited a 49% rate of protection against low-grade intraepithelial lesions (LSILs) and atypical squamous cells, not excluding high-grade squamous intraepithelial lesions (ASCH) or worse (LSIL/ASCH+), and a 100% rate of protection against high-grade squamous intraepithelial lesions (HSILs) or worse (HSIL+). Significant reductions in HPV16 (95%) and HPV18 (100%) infections were noted, but no differences were observed in HPV6 and HPV11 infections. The prevalences of HPV51 and HPV59 increased with vaccination, although these changes were not confirmed in the comparative study with J-HERS 2011. Comparing the prevaccination (J-HERS 2011) and postvaccination (J-HERS 2021) periods, 43%, 51%, 88%, and 62% reductions in HPV16, HPV18, HPV16/18, and HPV31/58 infection rates were observed, respectively. Similarly, 62% and 71% reductions in LSIL/ASCH+ and HSIL+ rates were noted, respectively. There were 88% and 87% reductions in LSIL/ASCH+ and HSIL+ rates in 16-21- and 28-33-year-old patients, respectively. Bivalent or quadrivalent vaccines provided 100% protection against high-grade squamous cell lesions (suggestive of CIN2 or CIN3) in young women aged <39 years at 9-12 years after initiation of Japan\'s first nationwide HPV vaccination program. Cross-protection against HPV31 and HPV58 is likely to occur, although some HPV-type replacements are inconsistent across vaccination regimens. This demonstrates the effectiveness of the HPV vaccine. However, continuous monitoring of cervical cancer and precancer is necessary in younger generations (born 1997-2007), who were rarely vaccinated due to the prolonged suspension of the vaccine recommendations in Japan.

Cervical cancer, a major health concern among women worldwide, is closely linked to human papillomavirus (HPV) infection. This study explores the evolving landscape of HPV molecular epidemiology in Taiwan over a decade (2010-2020), where prophylactic HPV vaccination has been implemented since 2007. Analyzing data from 40,561 vaginal swab samples, with 42.0% testing positive for HPV, we reveal shifting trends in HPV genotype distribution and infection patterns. The 12 high-risk genotypes, in order of decreasing percentage, were HPV 52, 58, 16, 18, 51, 56, 39, 59, 33, 31, 45, and 35. The predominant genotypes were HPV 52, 58, and 16, accounting for over 70% of cases annually. The proportions of high-risk and non-high-risk HPV infections varied across age groups. High-risk infections predominated in sexually active individuals aged 30-50 and were mixed-type infections. The composition of high-risk HPV genotypes was generally stable over time; however, HPV31, 33, 39, and 51 significantly decreased over the decade. Of the strains, HPV31 and 33 are shielded by the nonavalent HPV vaccine. However, no reduction was noted for the other seven genotypes. This study offers valuable insights into the post-vaccine HPV epidemiology. Future investigations should delve into HPV vaccines\' effects and their implications for cervical cancer prevention strategies. These findings underscore the need for continued surveillance and research to guide effective public health interventions targeting HPV-associated diseases.

BACKGROUND: The knowledge on vertical human papillomavirus (HPV) transmission is limited. We aimed to determine whether HPV transmission from parents to their offspring occurs before or during birth.
METHODS: Altogether, 321 mothers, 134 fathers, and their 321 newborn offspring from the Finnish Family HPV study cohort were included. Parents\' genital and oral brush samples and semen samples were collected for HPV testing at baseline (36 weeks of pregnancy). Oral, genital, and umbilical samples from the newborn and placenta samples were collected for HPV testing immediately after delivery. HPV risk for the newborn was calculated from the mother\'s and father\'s HPV status by using logistic regression analyses.
RESULTS: Concordances between mothers\' and their newborns\' HPV genotype at any site were statistically significant with HPV-6, -16, -18, -31, and -56; odds ratios (ORs) ranged from 3.41 (95% confidence interval [CI], 1.80-6.48) for HPV-16 to 634 (95% CI, 28.5-14 087) for HPV-31. Father-newborn HPV concordance was statistically significant with HPV-6 and HPV-31 (ORs, 4.89 [95% CI, 1.09-21.9] and 65.0 [95% CI, 2.92-1448], respectively).
CONCLUSIONS: The genotype-specific HPV concordance between parents and their newborn is suggestive for vertical HPV transmission. However, transmission from the father to the newborn remains more uncertain.

Human papillomavirus (HPV) type 31 (HPV31) is closely related to the most carcinogenic type, HPV16, but only accounts for 4% of cervical cancer cases worldwide. Viral genetic and epigenetic variations have been associated with carcinogenesis for other high-risk HPV types, but little is known about HPV31. We sequenced 2093 HPV31 viral whole genomes from two large studies, one from the U.S. and one international. In addition, we investigated CpG methylation in a subset of 175 samples. We evaluated the association of HPV31 lineages/sublineages, single nucleotide polymorphisms (SNPs) and viral methylation with cervical carcinogenesis. HPV31 A/B clade was >1.8-fold more associated with cervical intraepithelial neoplasia grade 3 and cancer (CIN3+) compared to the most common C lineage. Lineage/sublineage distribution varied by race/ethnicity and geographic region. A viral genome-wide association analysis identified SNPs within the A/B clade associated with CIN3+, including H23Y (C626T) (odds ratio = 1.60, confidence intervals = 1.17-2.19) located in the pRb CR2 binding-site within the E7 oncogene. Viral CpG methylation was higher in lineage B, compared to the other lineages, and was most elevated in CIN3+. In conclusion, these data support the increased oncogenicity of the A/B lineages and suggest variation of E7 as a contributing risk factor.

The Costa Rica HPV Vaccine Trial has documented cross-protection of the bivalent HPV vaccine against HPV31/33/45 up to 7 years after vaccination, even with one dose of the vaccine. However, the durability of such protection remains unknown. Here, we evaluate the efficacy of different schedules of the vaccine against HPV31/33/45 out to 11 years postvaccination, expanding to other nontargeted HPV types.
We compared the rates of HPV infection in vaccinated women with the rates in a comparable cohort of unvaccinated women. We estimated the average vaccine efficacy (VEavg) against incident infections and tested for a change in VE over time.
Among 3-dose women, we observed statistically significant cross-protection against HPV31/33/45 (VEavg = 64.4%, 95% confidence interval [CI] = 57.7% to 70.0%). Additionally, we observed borderline, statistically significant cross-protection against HPV35 (VEavg = 23.2%, 95% CI = 0.3% to 40.8%) and HPV58 (VEavg = 21.2%, 95% CI = 4.2% to 35.3%). There was no decrease in VE over time (two-sided Ptrend > .05 for HPV31, -33, -35, -45, and -58). As a benchmark, VEavg against HPV16/18 was 82.0% (95% CI = 77.3% to 85.7%). Among 1-dose women, we observed comparable efficacy against HPV31/33/45 (VEavg = 54.4%, 95% CI = 21.0% to 73.7%). Acquisition of nonprotected HPV types was similar between vaccinated and unvaccinated women, indicating that the difference in HPV infection rates was not attributable to differential genital HPV exposure.
Substantial cross-protection afforded by the bivalent vaccine against HPV31/33/45, and to a lesser extent, HPV35 and HPV58, was sustained and remained stable after 11 years postvaccination, reinforcing the notion that the bivalent vaccine is an effective option for protection against HPV-associated cancers.

OBJECTIVE: To evaluate the treatment effect of genital warts, we investigated the quadrivalent HPV vaccine injection compared with surgical excision.
METHODS: This prospective study included 26 patients (M:F = 24:2) who received HPV vaccine or surgical excision. After explanation of surgical excision or HPV vaccine, 16 patients underwent surgical excision and the others received HPV vaccine injections. Based on gross findings of genital warts, treatment outcomes were classified as complete response (no wart), partial response, and failed treatment.
RESULTS: Among enrolled patients, 42% (11 / 26) patients had recurrent genital warts. In vaccination group, complete response rates of genital wart were 60% following 3 times HPV vaccine. Partial response patients wanted to excise the genital lesions before the 3 times injection, because they worried about sexual transmission of disease to their sexual partners. One patient underwent surgical excision after 3 times injection. Excision sites included suprapubic lesions, but other sites including mid-urethra and glans showed complete response after injection. At a mean follow-up period of 8.42 ± 3.27 months, 10 patients (100%) who received HPV vaccine did not show recurrence.
CONCLUSIONS: The response rates after HPV vaccine injection were 90% (complete and partial). Our results suggested that HPV vaccines could be effective in management of genital warts.

Human papillomavirus (HPV) infection contributes to most cases of cervical cancer, and HPV genotypes exhibit different distributions according to geographic region. This study evaluates the prevalence of HPV infection in Hetian Prefecture, Xinjiang, and establishes risk factors associated with high-risk HPV (HR-HPV) genotypes in this region. In this cross-sectional, population-based study, 883 healthy women 15-54 years of age were enrolled. All participants completed a questionnaire regarding sociocultural and sexual activity characteristics. Visual inspections with acetic acid, colposcopies and biopsies were performed using the Preventive Oncology International microbiopsy protocol for pathological diagnosis. Cervical epithelial tissue specimens were collected and tested for HPV using linear array assays. According to the results of HR-HPV infection status, individuals infected with HR-HPV were classified into one group, and the remaining individuals were classified into the control group. The risk factors for HR-HPF infection were analyzed. The participants included 66 women (7.47%) with HR-HPV, 10 women (1.13%) with low-risk HPV, and 14 women (1.59%) with HPV of unknown risk. The five most prevalent types of HR-HPV were HPV-16 (0.31%), HPV-51 (0.08%), HPV-31 (0.07%), HPV-58 (0.07%), and HPV-39 (0.06%). Vulvovaginal ulcers and vulvovaginal inflammation were found in 190 participants (21.52%) and 256 participants (28.99%), respectively. The HR-HPV and control groups significantly differed with respect to age at first marriage, number of marriages, and the presence of vulvovaginal ulcers and vulvovaginal inflammation (p<0.05). Based on this study, an immunization strategy targeting HPV-16 should be prioritized in Hetian Prefecture. These findings contribute to the understanding of HPV infection.

BACKGROUND: The aetiological relationship between human papillomavirus (HPV) infection and cervical cancer (CC) is widely accepted. Our goal was to determine the prevalence of HPV types in Mexican women attending at the Mexican Institute for Social Security from different areas of Mexico.
METHODS: DNAs from 2,956 cervical samples were subjected to HPV genotyping: 1,020 samples with normal cytology, 931 with low-grade squamous intraepithelial lesions (LGSIL), 481 with high grade HGSIL and 524 CC.
RESULTS: Overall HPV prevalence was 67.1%. A total of 40 HPV types were found; HPV16 was detected in 39.4% of the HPV-positive samples followed by HPV18 at 7.5%, HPV31 at 7.1%, HPV59 at 4.9%, and HPV58 at 3.2%. HPV16 presented the highest prevalence both in women with altered or normal cytology and HPV 18 presented a minor prevalence as reported worldwide. The prevalence ratio (PR) was calculated for the HPV types. The analysis of PR showed that HPV16 presents the highest association with CC, HPV 31, -33, -45, -52 and -58 also demonstrating a high association.
CONCLUSIONS: The most prevalent HPV types in cervical cancer samples were -16, -18, -31, but it is important to note that we obtained a minor prevalence of HPV18 as reported worldwide, and that HPV58 and -52 also were genotypes with an important prevalence in CC samples. Determination of HPV genotypes is very important in order to evaluate the impact of vaccine introduction and future cervical cancer prevention strategies.

OBJECTIVE: Some studies suggest that Chlamydia trachomatis (CT) enhances cervical carcinogenesis; however, a possible confounding effect of persistent human papillomavirus (HPV) infection was not addressed. We examined the potential role of CT infection in the development of subsequent cervical intraepithelial neoplasia grade 3 or worse (CIN3+) in women with prevalent HPV infection and in a subgroup of women with persistent HPV infection.
METHODS: Participants in this population-based cohort study underwent a structured interview, including history of CT infection, and subsequently cervical exfoliated cells were obtained for HPV DNA and CT DNA testing. Women with high-risk HPV DNA infection and no prevalent cervical disease constituted the overall study population (n=1390). A subgroup of women with persistent HPV infection (n=320) was also identified. All women were passively followed for development of cervical lesions in the national Pathology Data Bank. HRs and 95% CIs for CIN3+ during follow-up (up to 19 years) were estimated in an accelerated failure time model.
RESULTS: Women who reported more than one CT infection had a statistically significantly increased risk of CIN3+ (high-risk HPV-positive, HR=2.51, 95% CI 1.44 to 4.37) (persistent HPV infection, HR=3.65, 95% CI 1.53 to 8.70). We found no association between CT DNA and subsequent risk of CIN3+ among women who were HPV-positive or had a persistent HPV infection at baseline.
CONCLUSIONS: Repeated CT infections increased the risk of CIN3+ among women with prevalent as well as persistent high-risk HPV infection.

OBJECTIVE: The aim of this study is to determine the rates of single and multiple type human papillomavirus (HPV) infection in women in the United States ages 31-65 with known cervical cytology results.
METHODS: Type-specific HPV analyses were conducted using the first samples of women who had HPV typing performed by Access Genetics as part of cervical cancer screening between July 2007 and May 2011. Women 31-65years at testing with associated abnormal cytology results were included. The odds of abnormal cytology (compared to normal results) for multiple vs. single HPV infections were calculated for each cytology sub-type and odds ratios (OR) and 95% confidence intervals (CI) are reported.
RESULTS: The analysis included 8182 women. The majority (67.7%) had ASCUS cervical cytology. A total of 329 (4.0%) were positive for 2 or more HPV types. For all cervical cytology subtypes considered (ASCUS, ASCUS-H, LSIL or HSIL), women with multiple type infections were more likely to have abnormal cytology (compared to normal cytology) with the highest OR associated with HSIL (OR 1.81 (1.26-2.60)). When analyzing HPV type 16 alone, women with multiple type infections were more likely to have abnormal cytology, with the highest OR associated with HSIL cytology (OR 2.98 (1.57-5.64)). Few women had HPV type 18 infections and no results reached statistical significance. Results based on phylogenic family organization focusing on the alpha 9 phylogenic family showed similar results as HPV type 16.
CONCLUSIONS: Women ages 31-65 with multiple type HPV infections were more likely to have abnormal cytology than those with single HPV type infections.