Cohort Profile: African Collaborative Center for Microbiome and Genomics Research's (ACCME's) Human Papillomavirus (HPV) and Cervical Cancer Study.
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ABSTRACT:
SUBMITTER: Adebamowo SN
PROVIDER: S-EPMC5837640 | biostudies-literature | 2017 Dec
REPOSITORIES: biostudies-literature
Publications
Cohort Profile: African Collaborative Center for Microbiome and Genomics Research's (ACCME's) Human Papillomavirus (HPV) and Cervical Cancer Study.
Adebamowo Sally N SN Dareng Eileen O EO Famooto Ayotunde O AO Offiong Richard R Olaniyan Olayinka O Obende Kayode K Adebayo Amos A Ologun Sanni S Alabi Bunmi B Achara Peter P Bakare Rasheed A RA Odutola Michael M Olawande Oluwatoyosi O Okuma James J Odonye George G Adebiyi Ruxton R Dakum Patrick P Adebamowo Clement A CA
International journal of epidemiology 20171201 6
Similar Datasets
Project description:African Collaborative Center for Microbiome and Genomics Research (ACCME) - CIDR
| PRJNA594428 | ENA
Project description:African Collaborative Center for Microbiome and Genomics Research (ACCME) - CIDR
| PRJNA594429 | ENA
Project description:Human papillomavirus (HPV) prevalence and genotype distribution data is important for HPV vaccine monitoring. This study investigated the prevalence and distribution of HPV genotypes in cervical lesions of unvaccinated women referred to Nelson Mandela Academic Hospital Gynaecology Department due to different abnormal cervical conditions. A total of 459 women referred to the Nelson Mandela Academic Hospital Gynaecology department were recruited. When the cervical biopsy was collected for histopathology, an adjacent biopsy was provided for HPV detection. Roche Linear Array HPV genotyping assay that detects 37 HPV genotypes was used to detect HPV infection in cervical biopsies. HPV infection was detected in 84.2% (383/455) of participants. The six most dominant HPV types were HPV-16 (34.7%), followed by HPV-35 (17.4%), HPV-58 (12.1%), HPV-45 (11.6%), HPV-18 (11.4%) and HPV-52 (9.7%). HPV-35 was the third most dominant type among women with cervical intraepithelial lesion (CIN)-2 (12.6%; single infection: 5.7% and multiple infection: 6.9%), the second most dominant type among women with CIN3 (22.2%; single infection: 8.0% and multiple infection: 14.2%); and the fourth most dominant type among women with cervical cancer (12.5%; single infection: 7.1% and multiple infection: 5.4%). A proportion of 41.1% (187/455) was positive for HPV types targeted by the Cervarix®, 42.4% (193/455) by Gardasil®4, and 66.6% (303/455) by Gardasil®9. There was a statistically significant increase when the prevalence of women infected with HPV-35 only or with other HPV types other than Gardasil®9 types was included to those infected with Gardasil®9 HPV types (66.6%, 303/455 increase to 76.0%, 346/455, p = 0.002). High HPV-35 prevalence in this population, especially among women with CIN3 warrants attention since it is not included in current commercially available HPV vaccines.
| S-EPMC8906620 | biostudies-literature
Project description:BackgroundHuman papillomavirus (HPV) is a necessary cause of cervical cancer, although some invasive cervical cancers may test negative by HPV PCR. We previously requested all invasive cervical cancers in Sweden during 10 years and subjected them to PCR. We also optimised methods for deep sequencing of formalin-fixed paraffin-embedded samples.MethodsUsing Novaseq 6000, we simultaneously sequenced total DNA and cDNA from 392 HPV PCR-negative cervical cancers. Non-human reads were queried against all known HPVs. The complete database now contains PCR and/or deep sequencing data on 2850 invasive cervical cancers.ResultsHPV sequences were detected in 169/392 of HPV PCR-negative cervical cancers. Overall, 30 different HPV types were detected, but only 5 types were present in proportions above 3% of cancers. More than 92% of tumours were HPV-positive in PCR and/or sequencing (95% confidence interval: 91.1-93.1%). Exploring possible reasons for failure to previously detect HPV suggest that more sensitive type-specific PCRs for HPV 31, 33, 45 and 73 targeting retained regions of HPV would have detected most of these (117/392).ConclusionsUnbiased deep sequencing provides comprehensive data on HPV types in cervical cancers and appears to be an important tool for quality assurance of HPV screening.
| S-EPMC7722749 | biostudies-literature
Project description:Differences in the cervicovaginal microbiome may influence the persistence of HPV and therefore, the progression to cervical cancer. We aimed to analyze and compare the metatranscriptome of cervical cancers positive for HPV 16 and 18 with those positive for other HPV types to understand the microbiome's influence on oncogenicity. RNA sequencing data from a total of 222 invasive cervical cancer cases (HPV16/18 positive (n=42) and HPV "Other types" (n=180)) were subjected to taxonomy classification (Kraken 2) including bacteria, virus and fungi to the level of species. With a median depth of 288,080.5 reads per sample, up to 107 species (38 bacterial, 16 viral and 53 fungal) were identified. Diversity analyses revealed no significant differences in viral or fungal species between HPV16/18 and other HPV types. Bacterial alpha diversity was significantly higher in the "Other HPV types" group for the Observed index (p=0.0074) (but not for Shannon). Cumulative species curves revealed greater species diversity in the "Other HPV types" group compared to "HPV16/18 but no significant differences in species abundance were found between HPV groups. The study did not detect strong significant microbiome differences between HPV 16/18 and other HPV types in cervical cancers. Further research is necessary to explore potential factors influencing the oncogenicity of different HPV types and their interaction with the cervical microbiome.
| S-EPMC11422507 | biostudies-literature
Project description:The association between human papillomavirus (HPV) DNA copy number and cervical disease was investigated. Viral DNA copy number for the most common high-risk HPV types in cervical cancer (types 16, 18, 31, and 45) was determined in cervical cytobrush specimens from 149 women with high-grade cervical intraepithelial neoplasias (CIN II-CIN III), 176 with low-grade CIN (CIN I), and 270 with normal cytology. Quantitative, PCR-based fluorescent assays for each of the HPV genotypes and for the beta-globin gene were used. The amount of cellular DNA increased significantly with increasing disease; thus, HPV was expressed as copies per microgram of cellular DNA. The assay had a dynamic range of >10(7), allowing documentation for the first time of the wide range of HPV copy numbers seen in clinical specimens. Median HPV DNA copy number varied by more than 10(4) among the viral types. HPV16 was present in the highest copy number; over 55% of HPV16-positive samples contained more than 10(8) copies/microgram. Median copy number for HPV16 showed dramatic increases with increasing epithelial abnormality, an effect not seen with the other HPV types. HPV16 increased from a median of 2.2 x 10(7) in patients with normal cytology, to 4.1 x 10(7) in CIN I patients, to 1.3 x 10(9) copies/microgram in CIN II-III patients. Even when stratified by cervical disease and viral type, the range of viral DNA copies per microgram of cellular DNA was quite large, precluding setting a clinically significant cutoff value for "high" copy numbers predictive of disease. This study suggests that the clinical usefulness of HPV quantitation requires reassessment and is assay dependent.
| S-EPMC88645 | biostudies-literature
Project description:Integration of human papillomavirus (HPV) viral DNA into the human genome has been postulated as an important etiological event during cervical carcinogenesis. Several recent reports suggested a possible role for such integration-targeted cellular genes (ITGs) in cervical carcinogenesis. Therefore, a comprehensive analysis of HPV integration events was undertaken using data collected from 14 publications, with 499 integration loci on human chromosomes included. It revealed that HPV DNA preferred to integrate into intragenic regions and gene-dense regions of human chromosomes. Intriguingly, the host cellular genes nearby the integration sites were found to be more transcriptionally active compared with control. Furthermore, analysis of the integration sites in the human genome revealed that there were several integration hotspots although all chromosomes were represented. The ITGs identified were found to be enriched in tumor-related terms and pathways using gene ontology and KEGG analysis. In line with this, three of six ITGs tested were found aberrantly expressed in cervical cancer tissues. Among them, it was demonstrated for the first time that MPPED2 could induce HeLa cell and SiHa cell G1/S transition block and cell proliferation retardation. Moreover, "knocking out" the integrated HPV fragment in HeLa cell line decreased expression of MYC located ∼500 kb downstream of the integration site, which provided the first experimental evidence supporting the hypothesis that integrated HPV fragment influence MYC expression via long distance chromatin interaction. Overall, the results of this comprehensive analysis implicated that dysregulation of ITGs caused by viral integration as possibly having an etiological involvement in cervical carcinogenesis.
| S-EPMC5057319 | biostudies-literature
Project description:Integration of human papillomavirus (HPV) DNA into the host genome can be a driver mutation in cervical carcinoma. Identification of HPV integration at base resolution has been a longstanding technical challenge, largely due to sensitivity masking by HPV in episomes or concatenated forms. The aim was to enhance the understanding of the precise localization of HPV integration sites using an innovative strategy. Using HPV capture technology combined with next generation sequencing, HPV prevalence and the exact integration sites of the HPV DNA in 47 primary cervical cancer samples and 2 cell lines were investigated. A total of 117 unique HPV integration sites were identified, including HPV16 (n = 101), HPV18 (n = 7), and HPV58 (n = 9). We observed that the HPV16 integration sites were broadly located across the whole viral genome. In addition, either single or multiple integration events could occur frequently for HPV16, ranging from 1 to 19 per sample. The viral integration sites were distributed across almost all the chromosomes, except chromosome 22. All the cervical cancer cases harboring more than four HPV16 integration sites showed clinical diagnosis of stage III carcinoma. A significant enrichment of overlapping nucleotides shared between the human genome and HPV genome at integration breakpoints was observed, indicating that it may play an important role in the HPV integration process. The results expand on knowledge from previous findings on HPV16 and HPV18 integration sites and allow a better understanding of the molecular basis of the pathogenesis of cervical carcinoma.
| S-EPMC4868726 | biostudies-literature
Project description:BackgroundThe objective of this study, the first of its kind in Kosovo, is to determine the level of Kosovo women's knowledge and awareness of HPV infection, HPV vaccination, and its relation to cervical cancer.MethodsThis cross-sectional study was conducted from July to October 2018 at the Clinic of Obstetrics and Gynecology at the Hospital and University Clinical Service of Kosovo.ResultsOut of 800 questionnaires distributed, 645 were completed and returned (80.6%). Only 0.5% of women were vaccinated against HPV. The majority of respondents (66.4%) had no previous knowledge of HPV (human papillomavirus). Only 27.6% of respondents were aware that HPV is responsible for cervical cancer. About two-thirds (70.1%) of respondents had never heard of the HPV vaccine, and only 24% knew that the HPV vaccine can prevent cervical cancer.ConclusionThe level of vaccination against HPV and the level of knowledge and awareness of HPV infection is extremely low. Higher education, younger age, and living in an urban area were favorable factors and correlated with awareness of HPV infection, vaccination against it, and its relation to cervical cancer. Based on this study, there is an immediate need for developing an educational program on HPV infection and the importance of HPV vaccination as a preventative measure against developing cervical cancer.
| S-EPMC8502331 | biostudies-literature
Project description:BackgroundHow vaginal infections such as bacterial vaginosis, Candida spp, and Trichomonas vaginalis affect persistence of human papillomavirus (HPV) infection is not well established. Our study aimed to evaluate the association between common vaginal infections and cervical non-HPV16/18 infection, as risk factors associated with persistence of nonvaccine HPV types will become increasingly relevant in the setting of HPV vaccination.MethodsWe performed an analysis in 2039 AS04-HPV16/18-vaccinated women enrolled in a phase II/III trial in China, who were HPV DNA negative at month 0 and 6 and had at least 1 subsequent follow-up visit. Vaginal infections were detected in liquid-based cytology according to the diagnostic criteria of the Bethesda System. Associations between vaginal infections and incident and 6-month persistent non-HPV16/18 infections in the cervix were evaluated using generalized estimating equations, adjusting for the age at initial vaccination, as well as HPV types in the persistence analysis.ResultsStudy visits with any vaginal infection had a statistically significant increased risk of incident non-HPV16/18 infection compared to those without vaginal infections (odds ratio [OR], 1.44 [95% confidence interval {CI}, 1.09-1.92]). However, vaginal infections were not associated with 6-month persistent non-HPV16/18 infection (OR, 1.02 [95% CI, .62-1.69]).ConclusionsOur study suggests that common vaginal infections are not associated with persistence of non-HPV16/18 infection among HPV16/18-vaccinated women.
| S-EPMC7982446 | biostudies-literature