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Background: HPV infection is the primary cause of cervical cancer, a leading cause of cancer among women in Kenya and many sub-Saharan African countries. High coverage of HPV vaccination is a World Health Organization priority to eliminate cervical cancer globally, but vaccine supply and logistics limit widespread implementation of the current two or three dose HPV vaccine schedule.Methods: We are conducting an individual randomized controlled trial to evaluate whether a single dose of the bivalent (HPV 16/18) or nonavalent (HPV 16/18/31/33/45/52/58/6/11) HPV vaccine prevents persistent HPV infection, a surrogate marker for precancerous lesions and cervical cancer. The primary objective is to compare the efficacy of immediate, single-dose bivalent or nonavalent vaccination with delayed HPV vaccination. Kenyan women age 15-20 years old are randomized to immediate bivalent HPV and delayed meningococcal vaccine (group 1), immediate nonavalent HPV vaccine and delayed meningococcal vaccine (group 2), or immediate meningococcal vaccine and delayed HPV vaccine (group 3) with 36 months of follow-up. The primary outcome is persistent vaccine-type HPV infection by month 18 and by month 36 for the final durability outcome. The secondary objectives include to (1) evaluate non-inferiority of antibody titers among girls and adolescents (age 9 to 14 years) from another Tanzanian study, the DoRIS Study (NCT02834637), compared to KEN SHE Study participants; (2) assess the memory B cell immune response at months 36 and 37; and (3) estimate cost-effectiveness using the trial results and health economic models.Discussion: This study will evaluate single-dose HPV vaccine efficacy in Africa and has the potential to guide public health policy and increase HPV vaccine coverage. The secondary aims will assess generalizability of the trial results by evaluating immunobridging from younger ages, durability of the immune response, and the long-term health benefits and cost of single-dose HPV vaccine delivery.Trial Registration: ClinicalTrials.gov NCT03675256 . Registered on September 18, 2018. [ABSTRACT FROM AUTHOR]

Background Little is known about the epidemiology of β and γ human papillomaviruses (HPVs) in oral cavities of healthy women. Methods We performed multiplex polymerase chain reaction analysis for detection of 46 β-HPVs and 51 γ-HPVs in stored oral rinse samples from healthy mid-adult women (age, 30–50 years). A total of 407 women were tested for β-HPVs, and 310 were tested for γ-HPVs. We used log-binomial regression to identify determinants of β-HPV and γ-HPV in separate models. Using paired fingernail data from a subset of 184 women, we also evaluated whether fingernail β-HPV detection was associated with concurrent detection of the same type in the oral cavity. Results Oral HPV prevalence was 20.6% for β-HPV and 10.7% for γ-HPV. In multivariate analysis, oral β-HPV detection was associated with increasing age (adjusted prevalence ratio [aPR] per 5-year difference, 1.37; 95% confidence interval [CI], 1.01–1.86) and a greater lifetime number of oral sex partners (aPR for reporting ≥6 vs 0–5 partners, 2.06; 95% CI, 1.01–4.20). In a separate model, concurrent detection of the same β-HPV type in fingernails was strongly associated with oral β-HPV detection (aPR, 31.44; 95% CI, 19.81–49.49). No significant determinants of γ-HPV detection were identified. Conclusions Our results suggest a sexual transmission route for β-HPVs and support the hypothesis that fingers may serve as a source of transmission or autoinoculation of β-HPVs to the oral cavity. [ABSTRACT FROM AUTHOR]

Background High-risk human papillomavirus (hrHPV) causes cervical cancer. In the United States, approximately 40% of women aged 14–59 years from all racial and ethnic groups are infected with HPV, and prevalence typically declines with age. However, American Indian (AI) women are insufficiently sampled to permit a population-specific estimate of hrHPV prevalence. Methods Vaginal swabs were self-collected by 698 AI women aged 21–65 years from a tribal community in the Great Plains. We estimated the population prevalence of hrHPV and identified predominant genotypes. Results The combined prevalence of hrHPV genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68 was 34.8%. HPV-51 (7.6%), HPV-58 (5.3%), HPV-52 (4.3%), HPV-18 (4.3%), and HPV-16 (3.9%) were most prevalent. hrHPV prevalence declined with age, from 42.2% in women aged 21–24 years to 27.9% in women aged 50–65 years. Conclusions HPV-51 was the single most prevalent oncogenic genotype. The combined prevalence of hrHPV among AI women in our sample was high, particularly among women aged 50–65 years, for whom hrHPV prevalence was approximately triple that of other races. Cervical cancer screening efforts should be increased, particularly among women from the community aged 30 years and older. [ABSTRACT FROM AUTHOR]

Background: Antiretroviral therapy for HIV-2 infection is hampered by intrinsic resistance to many of the drugs used to treat HIV-1. Limited studies suggest that the integrase inhibitors (INIs) raltegravir and elvitegravir have potent activity against HIV- 2 in culture and in infected patients. There is a paucity of data on genotypic variation in HIV-2 integrase that might confer intrinsic or transmitted INI resistance. Methods: We PCR amplified and analyzed 122 HIV-2 integrase consensus sequences from 39 HIV-2-infected, INI-naive adults in Senegal, West Africa. We assessed genetic variation and canonical mutations known to confer INI-resistance in HIV-1. Results: No amino acid-altering mutations were detected at sites known to be pivotal for INI resistance in HIV-1 (integrase positions 143, 148 and 155). Polymorphisms at several other HIV-1 INI resistance-associated sites were detected at positions 72, 95, 125, 154, 165, 201, 203, and 263 of the HIV-2 integrase protein. Conclusion: Emerging genotypic and phenotypic data suggest that HIV-2 is susceptible to the new class of HIV integrase inhibitors. We hypothesize that intrinsic HIV-2 integrase variation at ''secondary'' HIV-1 INI-resistance sites may affect the genetic barrier to HIV-2 INI resistance. Further studies will be needed to assess INI efficacy as part of combination antiretroviral therapy in HIV-2-infected patients. [ABSTRACT FROM AUTHOR]

The article offers a study which examines baseline human papillomavirus (HPV) 16 and HPV18 DNA load among women with and without concurrent coinfection with other HPV types. The study depicts that lower HPV16 and HPV18 DNA load was associated with coinfection with other HPV types. It is stated that species-specific association may in part reflect differences in the extent of cross-reaction of cellular immune response induced by other types.

Background: High-risk human papillomavirus (hrHPV) causes cervical cancer. In the United States, approximately 40% of women aged 14-59 years from all racial and ethnic groups are infected with HPV, and prevalence typically declines with age. However, American Indian (AI) women are insufficiently sampled to permit a population-specific estimate of hrHPV prevalence.Methods: Vaginal swabs were self-collected by 698 AI women aged 21-65 years from a tribal community in the Great Plains. We estimated the population prevalence of hrHPV and identified predominant genotypes.Results: The combined prevalence of hrHPV genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68 was 34.8%. HPV-51 (7.6%), HPV-58 (5.3%), HPV-52 (4.3%), HPV-18 (4.3%), and HPV-16 (3.9%) were most prevalent. hrHPV prevalence declined with age, from 42.2% in women aged 21-24 years to 27.9% in women aged 50-65 years.Conclusions: HPV-51 was the single most prevalent oncogenic genotype. The combined prevalence of hrHPV among AI women in our sample was high, particularly among women aged 50-65 years, for whom hrHPV prevalence was approximately triple that of other races. Cervical cancer screening efforts should be increased, particularly among women from the community aged 30 years and older. [ABSTRACT FROM AUTHOR]

BACKGROUND: Single-dose human papillomavirus (HPV) vaccination, if efficacious, would be tremendously advantageous, simplifying implementation and decreasing costs. METHODS: We performed a randomized, multicenter, double-blind, controlled trial of single-dose nonavalent (HPV 16/18/31/33/45/52/58/6/11 infection) or bivalent (HPV 16/18 infection) HPV vaccination compared with meningococcal vaccination among Kenyan women 15 to 20 years of age. Enrollment and 6-monthly cervical swabs and a month 3 vaginal swab were tested for HPV deoxyribonucleic acid (DNA). Enrollment sera were tested for HPV antibodies. The modified intent-to-treat (mITT) cohort comprised participants who had an HPV antibody-negative result at enrollment and an HPV DNA-negative result at enrollment and month 3. The primary outcome was incident persistent vaccine-type HPV infection by month 18. RESULTS: Between December 2018 and June 2021, 2275 women were randomly assigned and followed. A total of 758 participants received the nonavalent HPV vaccine, 760 received the bivalent HPV vaccine, and 757 received the meningococcal vaccine; retention was 98%. Thirty-eight incident persistent infections were detected in the HPV 16/18 mITT cohort: one each among participants assigned to the bivalent and nonavalent groups and 36 among those assigned to the meningococcal group. Nonavalent vaccine efficacy (VE) was 97.5% (95% confidence interval [CI], 81.7 to 99.7%; P≤0.0001), and bivalent VE was 97.5% (95% CI, 81.6 to 99.7%; P≤0.0001). Thirty-three incident persistent infections were detected in the HPV 16/18/31/33/45/52/58 mITT cohort: four in the nonavalent group and 29 in the meningococcal group. Nonavalent VE for HPV 16/18/31/33/45/52/58 was 88.9% (95% CI, 68.5 to 96.1; P<0.0001). The rate of serious adverse events was 4.5% to 5.2% by group. CONCLUSIONS: Over the 18-month timeframe we studied, single-dose bivalent and nonavalent HPV vaccines were each highly effective in preventing incident persistent oncogenic HPV infection, similar to multidose regimens. (Funded by the National Institutes of Health, the Bill and Melinda Gates Foundation, and the University of Washington; ClinicalTrials.gov number, NCT03675256.), (Copyright: © 2022 Author(s), Massachusetts Medical Society. All rights reserved.)

More than 100 human papillomavirus (HPV) types have been identified, and over 40 of them infect the anogenital epithelium. Because each HPV type is associated with different risks for the development of cervical cancer, detecting and genotyping HPVs has increasingly become an integral part of cervical cancer control. Here, we describe a Luminex assay-based liquid bead microarray assay for genotyping 37 HPV types, which is objective, scalable, amenable to a high-throughput configuration, and has the potential to be automated.