Academic literature on the topic 'HPV-18 LCR'
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Journal articles on the topic "HPV-18 LCR"
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Wyant, Patrícia Soares, Daniela Marreco Cerqueira, Daniella Sousa Moraes, José Paulo Gagliardi Leite, Cláudia Renata Fernandes Martins, Marcelo de Macedo Brígido, and Tainá Raiol. "Phylogeny and Polymorphism in the Long Control Region, E6, and L1 of Human Papillomavirus Types 53, 56, and 66 in Central Brazil." International Journal of Gynecologic Cancer 21, no. 2 (January 2011): 222–29. http://dx.doi.org/10.1097/igc.0b013e318208c73d.
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Introduction:Several studies related that different human papillomavirus (HPV) types and intratype variants can present different oncogenic potential. In opposite to HPVs 16 and 18 variants, information about variants of other carcinogenic HPV types is still scarce. The aim of this study was to investigate the genetic variability of HPVs 53, 56, and 66 from Central Brazil isolates.Methods:The long control region (LCR), E6, and L1 genomic regions were amplified and sequenced. We evaluate for nucleotide variations in relation to the reference sequence of each HPV type and also the conservation of physicochemical properties of the deduced amino acid substitutions. In silico analysis was performed to locate binding sites for transcriptional factors within the LCR. Moreover, we performed a phylogenetic analysis with the Central Brazilian and worldwide sequences available at genomic databases.Results:Gathering LCR, E6, and L1 genomic regions, the highest genetic variability was found among HPV-53 isolates with 52 nucleotide variations, followed by HPVs 56 and 66 with 24 and 16 nucleotide substitutions, respectively. The genetic analysis revealed 11 new molecular variants of all HPV types analyzed, totalizing 31 new nucleotide and 3 new amino acid variations. Eight nonconservative amino acid substitutions were detected, which may indicate a biological and pathogenic diversity among HPV types. Furthermore, 8 nucleotide substitutions were localized at putative binding sites for transcription factors in the LCR with a potential implication on viral oncogene expression. The HPVs 53, 56, and 66 phylogenetic analysis confirmed a dichotomic division only described to HPV subtypes and different from the patterns described for HPVs 16 and 18 variants.Conclusions:The high genetic variability observed emphasizes the importance of investigating polymorphisms in types other than HPVs 16 or 18 to better understand the molecular genomic profile of viral infection by different HPV types.
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Stünkel, Walter, and Hans-Ulrich Bernard. "The Chromatin Structure of the Long Control Region of Human Papillomavirus Type 16 Represses Viral Oncoprotein Expression." Journal of Virology 73, no. 3 (March 1, 1999): 1918–30. http://dx.doi.org/10.1128/jvi.73.3.1918-1930.1999.
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ABSTRACT The long control region (LCR) of human papillomavirus type 16 (HPV-16) has a size of 850 bp (about 12% of the viral genome) and regulates transcription and replication of the viral DNA. The 5′ segment of the LCR contains transcription termination signals and a nuclear matrix attachment region, the central segment contains an epithelial cell-specific enhancer, and the 3′ segment contains the replication origin and the E6 promoter. Here we report observations on the chromatin organization of this part of the HPV-16 genome. Treatment of the nuclei of CaSki cells, a cell line with 500 intrachromosomal copies of HPV-16, with methidiumpropyl-EDTA-Fe(II) reveals nucleosomes in specific positions on the LCR and the E6 and E7 genes. One of these nucleosomes, which we termed Ne, overlaps with the center of the viral enhancer, while a second nucleosome, Np16, overlaps with the replication origin and the E6 promoter. The two nucleosomes become positioned on exactly the same segments after in vitro assembly of chromatin on the cloned HPV-16 LCR. Primer extension mapping of DNase I-cleaved chromatin revealed Np16 to be positioned centrally over E6 promoter elements, extending into the replication origin. Ne covers the center of the enhancer but leaves an AP-1 site, one of the strongestcis-responsive elements of the enhancer, unprotected. Np16, or a combination of Np16 and Ne, represses the activity of the E6 promoter during in vitro transcription of HPV-16 chromatin. Repression is relieved by addition of Sp1 and AP-1 transcription factors. Sp1 alters the structure of Np16 in vitro, while no changes can be observed during the binding of AP-1. HPV-18, which has a similar arrangement ofcis-responsive elements despite its evolutionary divergence from HPV-16, shows specific assembly in vitro of a nucleosome, Np18, over the E1 binding site and E6 promoter elements but positioned about 90 bp 5′ of the position of Np16 on the homologous HPV-16 sequences. The chromatin organization of the HPV-16 and HPV-18 genomes suggests important regulatory roles of nucleosomes during the viral life cycle.
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Díaz-Tejeda, Yakelin, Miriam C. Guido-Jiménez, Helga López-Carbajal, Alfredo Amador-Molina, Rocío Méndez-Martínez, Patricio Gariglio-Vidal, Marcela Lizano, and Alejandro García-Carrancá. "Nanog, in Cooperation with AP1, Increases the Expression of E6/E7 Oncogenes from HPV Types 16/18." Viruses 13, no. 8 (July 28, 2021): 1482. http://dx.doi.org/10.3390/v13081482.
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Persistent infections with some types of human papillomavirus (HPV) constitute the major etiological factor for cervical cancer development. Nanog, a stem cell transcription factor has been shown to increase during cancer progression. We wanted to determine whether Nanog could modulate transcription of E6 and E7 oncogenes. We used luciferase reporters under the regulation of the long control region (LCR) of HPV types 16 and 18 (HPV16/18) and performed RT-qPCR. We found that Nanog increases activity of both viral regulatory regions and elevates endogenous E6/E7 mRNA levels in cervical cancer-derived cells. We demonstrated by in vitro mutagenesis that changes at Nanog-binding sites found in the HPV18 LCR significantly inhibit transcriptional activation. Chromatin immunoprecipitation (ChIP) assays showed that Nanog binds in vivo to the HPV18 LCR, and its overexpression increases its binding as well as that of c-Jun. Surprisingly, we observed that mutation of AP1-binding sites also affect Nanog’s ability to activate transcription, suggesting cooperation between the two factors. We searched for putative Nanog-binding sites in the LCR of several HPVs and surprisingly found them only in those types associated with cancer development. Our study shows, for the first time, a role for Nanog in the regulation of E6/E7 transcription of HPV16/18.
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Amador-Molina, Alfredo, José Luis González-Montoya, Alejandro García-Carrancá, Alejandro Mohar, and Marcela Lizano. "Intratypic changes of the E1 gene and the long control region affect ori function of human papillomavirus type 18 variants." Journal of General Virology 94, no. 2 (February 1, 2013): 393–402. http://dx.doi.org/10.1099/vir.0.045807-0.
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A persistent infection with high-risk human papillomavirus (HPV) constitutes the main aetiological factor for cervical cancer development. HPV16 and 18 are the most prevalent types found in cervical cancer worldwide. It has been proposed that HPV intratype variations may result in differences in biological behaviour. Three different HPV18 variants belonging to the Asian Amerindian (AsAi), European (E) and African (Af) branches have been associated with specific histological types of cervical cancer with different relative prognoses, suggesting that HPV18 genomic variations might participate in disease evolution. The E1 viral protein plays a critical role in controlling viral replication and load, requiring interaction with the E2 protein to bind to the long control region (LCR). In this work, we analysed if intratype variations in the LCR and E1 and E2 genes of HPV18 impact ori replication. While the changes found in E2 genes of the tested variants were irrelevant in replication, we found that variations in E1 and LCR in fact affect ori function. It was demonstrated that nucleotide differences in the LCR variants impact ori function. Nevertheless, HPV18 E1 Af gene was mainly involved in the highest ori replication, compared with the E and AsAi E1 variants. Immunofluorescence analysis showed increased levels of Af E1 in the nucleus, correlating with the enhanced ori function. Site-directed mutagenesis revealed that at least two positions in the N-terminal domain of E1 could impact its nuclear accumulation.
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Lina Villa, Luisa, and Richard Schlegel. "Differences in transformation activity between HPV-18 and HPV-16 map to the viral LCR-E6-E7 region." Virology 181, no. 1 (March 1991): 374–77. http://dx.doi.org/10.1016/0042-6822(91)90507-8.
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Martínez, Rocio Susana Méndez, Norma Rivera-Martínez, Juan G. Sierra-Madero, David Cantú de León, and Alejandro García-Carranca. "23. Prevalence of virus infection of human papillomavirus and identification of variants in the anal canal of men who have sex with men HIV-positive in Mexico." Sexual Health 10, no. 6 (2013): 581. http://dx.doi.org/10.1071/shv10n6ab23.
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Background Men who have sex with men (MSM) have been identified as a high-risk group for anal cancer. HPV has been found associated with this neoplasia as it has been in cervical cancer. Concurrent infection with HIV may facilitate or accelerate the pathological consequences of HPV infections. In Mexico, where cervical cancer is a major public health problem, little is known about the prevalence of anal cancer and the role of HPV in the HIV-positive population of MSM. Methods: We analysed 323 anal exudates from HIV-positive MSM, from the HIV Clinic at Instituto Nacional de Ciencias Médicas y Nutrición ‘Salvador Zubirán’, in Mexico City. Extraction and purification of DNA was performed with the Genomics Wizard kit (Promega), HPV detection was performed by PCR using primers MY09/11. All negative samples underwent a PCR for identification of fragment of the β-globin gene to check DNA integrity. Positive samples were subjected to PCR using specific primers for E6 of type 16, and the LCR from type 18. The identification of variants was determined by sequencing the E6 gene and the LCR of 40 samples positive for HPV type 16, using the Big Dye terminator kit and AB Prism 3100. We used INNO-LiPA HPV Genotyping Extra kit (INNOGENETICS), for the identification of 28 different types of HPV using SPF10 primers in these samples. Results: The prevalence of HPV in the anal epithelium of 323 patients was high (86%). 28% were positive for type 16, and 9% for type 18. Among those patients who were type 16+, all except one were co-infected with other HPV types that included 21 different types present in the following order: 11, 51, 52, 66, 68, 74, 18, 45, 35, 26, 44, 70, 53, 54, 82, 31, 33, 56, 58, 59. In addition, in these patients, European variants were the most prevalent, followed by Asian American ones. Conclusions: The prevalence of HPV was high in the anal canal of a group of 323 HIV+ MSM in Mexico City. A group of 40 HPV16-positive patients showed multiple co-infections with other different HPV types. In addition, European variants of type 16 were the most prevalent. This study emphasises the need for an early detection of HPV infections in the anal canal of MSM who are positive for HIV in order to avoid progression to anal neoplasia.
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Munsamy, Yuri, Riaz Y. Seedat, Tumelo R. Sekee, Phillip A. Bester, and Felicity J. Burt. "Complete genome sequence of a HPV31 isolate from laryngeal squamous cell carcinoma and biological consequences for p97 promoter activity." PLOS ONE 16, no. 8 (August 25, 2021): e0252524. http://dx.doi.org/10.1371/journal.pone.0252524.
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Human papillomavirus type 31, although detected less frequently than HPV types 16 and 18, is associated with head and neck squamous cell carcinomas. Previous studies suggest that polymorphisms in the long control region (LCR) may alter the oncogenic potential of the virus. This study reports the first complete genome of a South African HPV31 isolate from a laryngeal squamous cell carcinoma. Sequence variations relative to the HPV31 prototype sequence were identified. The pBlue-Topo® vector, a reporter gene system was used to investigate the possible influence of these variations on the LCR promoter activity in vitro. Using mutagenesis to create two different fragments, β-galactosidase assays were used to monitor the effect of nucleotide variations on the p97 promoter. Increased β-galactosidase expression was observed in mutants when compared to the South African HPV31 LCR isolate. Enhanced transcriptional activity was observed with the mutant that possessed a single nucleotide change within the YY1 transcription factor binding site. In conclusion, sequence variation within the LCR of HPV31 isolates may have a functional effect on viral p97 promoter activity.
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Tan, Shyh-Han, Dusan Bartsch, Elisabeth Schwarz, and Hans-Ulrich Bernard. "Nuclear Matrix Attachment Regions of Human Papillomavirus Type 16 Point toward Conservation of These Genomic Elements in All Genital Papillomaviruses." Journal of Virology 72, no. 5 (May 1, 1998): 3610–22. http://dx.doi.org/10.1128/jvi.72.5.3610-3622.1998.
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ABSTRACT The gene functions, transcriptional regulation, and genome replication of human papillomaviruses (HPVs) have been extensively studied. Thus far, however, there has been little research on the organization of HPV genomes in the nuclei of infected cells. As a first step to understand how chromatin and suprachromatin structures may modulate the life cycles of these viruses, we have identified and mapped interactions of HPV DNAs with the nuclear matrix. The endogenous genomes of HPV type 16 (HPV-16) which are present in SiHa, HPKI, and HPKII cells, adhere in vivo to the nuclear matrixes of these cell lines. A tight association with the nuclear matrix in vivo may be common to all genital HPV types, as the genomes of HPV-11, HPV-16, HPV-18, and HPV-33 showed high affinity in vitro to preparations of the nuclear matrix of C33A cells, as did the well-known nuclear matrix attachment region (MAR) of the cellular beta interferon gene. Affinity to the nuclear matrix is not evenly spread over the HPV-16 genome. Five genomic segments have strong MAR properties, while the other parts of the genome have low or no affinity. Some of the five MARs correlate with known cis-responsive elements: a strong MAR lies in the 5′ segment of the long control region (LCR), and another one lies in the E6 gene, flanking the HPV enhancer, the replication origin, and the E6 promoter. The strongest MAR coincides with the E5 gene and the early-late intergenic region. Weak MAR activity is present in the E1 and E2 genes and in the 3′ part of L2. The in vitro map of MAR activity appears to reflect MAR properties in vivo, as we found for two selected fragments with and without MAR activity. As is typical for many MARs, the two segments with highest affinity, namely, the 5′ LCR and the early-late intergenic region, have an extraordinarily high A-T content (up to 85%). It is likely that these MARs have specific functions in the viral life cycle, as MARs predicted by nucleotide sequence analysis, patterns of A-T content, transcription factor YY1 binding sites, and likely topoisomerase II cleavage sites are conserved in similar positions throughout all genital HPVs.
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Chen, Alyce A., Tarik Gheit, Silvia Franceschi, Massimo Tommasino, and Gary M. Clifford. "Human Papillomavirus 18 Genetic Variation and Cervical Cancer Risk Worldwide." Journal of Virology 89, no. 20 (August 12, 2015): 10680–87. http://dx.doi.org/10.1128/jvi.01747-15.
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ABSTRACTHuman papillomavirus 18 (HPV18) is the second most carcinogenic HPV type, after HPV16, and it accounts for approximately 12% of squamous cell carcinoma (SCC) as well as 37% of adenocarcinoma (ADC) of the cervix worldwide. We aimed to evaluate the worldwide diversity and carcinogenicity of HPV18 genetic variants by sequencing the entire long control region (LCR) and the E6 open reading frame of 711 HPV18-positive cervical samples from 39 countries, taking advantage of the International Agency for Research on Cancer biobank. A total of 209 unique HPV18 sequence variants were identified that formed three phylogenetic lineages (A, B, and C). A and B lineages each divided into four sublineages, including a newly identified candidate B4 sublineage. The distribution of lineages varied by geographical region, with B and C lineages found principally in Africa. HPV18 (sub)lineages were compared between 453 cancer cases and 236 controls, as well as between 81 ADC and 160 matched SCC cases. In region-stratified analyses, there were no significant differences in the distribution of HPV18 variant lineages between cervical cancer cases and controls or between ADC and SCC. In conclusion, our findings do not support the role of HPV18 (sub)lineages for discriminating cancer risk or explaining why HPV18 is more strongly linked with ADC than SCC.IMPORTANCEThis is the largest and most geographically/ethnically diverse study of the genetic variation of HPV18 to date, providing a comprehensive reference for phylogenetic classification of HPV18 sublineages for epidemiological and biological studies.
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Turner, S., C. Studwell, S. Deharvengt, K. D. Lyons, J. A. Plata, E. LaRochelle, A. M. Zapata, L. Kennedy, and S. Bejarano. "High-Risk HPV Genotypes Identified in Northern Honduras: Evidence for Prevention." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 211s. http://dx.doi.org/10.1200/jgo.18.85200.
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Background: Cervical cancer is one of the most prevalent cancers in Honduran women. Lacking national or population-based registries, we rely on hospital registries to establish incidence: San Felipe General Hospital in 2012 diagnosed 38% of 998 women and The League against Cancer Hospital (LCC) in 2016 diagnosed 54.4% of 695 women with cervical cancer CC. According to PAHO's Honduras Profile 2013, screening coverage with Pap was 48.1%. Bruni in 2010 reported a prevalence of high risk HPV (hrHPV) infection for Central America of 13%, identifying genotypes 16, 18, 52, 31 and 58 as most frequent. Information about pathogenesis of hrHPV to induce cervical lesions is based on models of genotypes 16 and 18 only. Aim: Inform evidence of hrHPV genotypes collected in Honduras from an urban and a rural population, generate discussion and subsequent improvement of cervical cancer control strategies in our country. Methods: In 2016, 2 clinical studies funded by Norris Cotton Cancer Center at Dartmouth College and the LCC accrued 913 women: 401 in Locomapa Valley (rural), 111 in La Mosquitia (remote rural), and 401 in a textile factory in San Pedro Sula (urban). Women were consented, to obtain 3 cervical samples, during a cervical cancer screening brigade. One sample for conventional cytology, and 2 for hrHPV by PCR genotyping. One local with our customized PCR device and the second at Dartmouth. An educational component and survey were included. Positive patients identified with hrHPV, pre or invasive cancer were referred to LCC for treatment and follow-up. Results: In Locomapa and the factory (rural and urban sites) 13% of participants were positive for hrHPV. Only 15% had HPV 16. The following common genotypes varied by location: urban factory HPV 59, 12% in rural location HPV 58, 10%; HPV 31, 9%; HPV 39 8%; HPV 35 and 66, 7%; HPV 45 and 51, 6%; HPV 18 and 56, 3%; HPV 33 and 52, 1%. 17% of women had multiple hrHPV coinfection. 7.7% had abnormal Pap tests. In La Mosquitia (remote rural), 24% of women were positive for hrHPV: HPV 52, 29%; HPV 16, 23%; HPV 39, 10%; HPV 68, 6%; HPV 58, 6%; HPV 45, 6%; HPV 51 and HPV 31, 18, 66, 59 and 35, 3% each. 1.8% had abnormal Pap tests; all participants identified with hrHPV were referred for follow-up. The average age was 40.3 years, parity, 3 children, education 6.0 years; and 15% were first-time users of a cervical screening program. Conclusion: Associate the burden of disease, with risk factors, will help us to generate models of prevention and care that are reproducible and effective to reduce morbi-mortality. Brigade-type screening models, with trained providers working at a community location over a single day, can offer improved access for women at risk and facilitate educational activities for health promotion. Introducing tests as hrHPV DNA detection, effectively reduces the volume of women to follow. Strengthening the capacity of primary care with novel screening techniques and ensure diligent follow-up is essential.
Dissertations / Theses on the topic "HPV-18 LCR"
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Lung, Mandy Siu Yu Biotechnology & Biomolecular Sciences Faculty of Science UNSW. "The use of Human Papillomavirus promoters to target Cervical Cancer cells." Publisher:University of New South Wales. Biotechnology & Biomolecular Sciences, 2008. http://handle.unsw.edu.au/1959.4/42610.
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Human Papillomavirus (HPV) is one of the most common causes of sexually transmitted disease worldwide. Infections by high-risk HPVs, such as HPV-18, have been associated etiologically with cervical cancer. The successful development of HPV vaccines may be beneficial to the HPV-na??ve population, but women that have already been exposed to the virus are still at risk of developing HPV-associated malignancies. A need for a systemic cure for HPV-infection therefore still exists. Gene therapies using tissue-specific promoters have been reported to be a promising tool for treating cancers; however, few studies have explored this possibility for cervical cancer. The aim of this project is to construct a gene expression vector that can specifically target HPV-infected cervical cancer cells, by making use of the activity and selectivity of the P105 promoter which is determined by transcription control elements within the HPV-18 long control region (LCR). The first part of this study involved the construction of LCR deletion plasmids, and examining the subsequent level of gene expression induced within different mammalian cell lines. The results suggest the LCR to be capable in achieving cervical cancer-specific gene expression. The 3′-end of the viral L1 gene upstream of the LCR appeared to have a repressive effect on the promoter and therefore should be excluded for maximum LCR promoter activity. The second part of the project involved site-directed mutagenesis studies performed on selected transcription factor binding sites with an attempt to further increase the level of LCR promoter activity and specificity towards HPV-infected cervical cancer cells. The results suggest that a GRE/YY1 mutation may significantly enhance promoter activity. In terms of promoter regulation, the E2BSs appeared to be responsible for promoter activation in the absence of viral E2 proteins. The findings of this study suggest a possible gene therapy approach towards the treatment of cervical cancer. By making use of the activity and specificity of the HPV-18 P105 promoter to induce cervical carcinoma-specific expression of appropriate therapeutic genes, suicidal phenotypes can be introduced selectively within HPV-positive cervical cancer cells while normal HPV-negative cells are unaffected.