The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform
Zigui Chen - One of the best experts on this subject based on the ideXlab platform.
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Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
2018Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Charles E. Wood, Julio C. Ruiz, Gary M. Clifford, Paul K. S. Chan, Robert D BurkAbstract:Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
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Degradation of p53 by Human Alphapapillomavirus E6 Proteins Shows a Stronger Correlation with Phylogeny than
2013Co-Authors: Koenraad Van Doorslaer, Zigui Chen, Tutik Ristriani, Murielle Masson, Gilles Travé, Robert D BurkAbstract:Background: Human Papillomavirus (HPV) E6 induced p53 degradation is thought to be an essential activity by which highrisk human Alphapapillomaviruses (alpha-HPVs) contribute to cervical cancer development. However, most of our understanding is derived from the comparison of HPV16 and HPV11. These two viruses are relatively distinct viruses, making the extrapolation of these results difficult. In the present study, we expand the tested strains (types) to include members of all known HPV species groups within the Alphapapillomavirus genus. Principal Findings: We report the biochemical activity of E6 proteins from 27 HPV types representing all alpha-HPV species groups to degrade p53 in human cells. Expression of E6 from all HPV types epidemiologically classified as group 1 carcinogens significantly reduced p53 levels. However, several types not associated with cancer (e.g., HPV53, HPV70 and HPV71) were equally active in degrading p53. HPV types within species groups alpha 5, 6, 7, 9 and 11 share a most recent common ancestor (MRCA) and all contain E6 ORFs that degrade p53. A unique exception, HPV71 E6 ORF that degraded p53 was outside this clade and is one of the most prevalent HPV types infecting the cervix in a population-based study of 10,000 women. Alignment of E6 ORFs identified an amino acid site that was highly correlated with the biochemical ability to degrade p53. Alteration of this amino acid in HPV71 E6 abrogated its ability to degrade p53, while alteration of this site in HPV71-related HPV90 and HPV106 E6s enhanced their capacity to degrade p53
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evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes hpv18 hpv39 hpv45 hpv59 hpv68 and hpv70
PLOS ONE, 2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.
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Evolution and Taxonomic Classification of Alphapapillomavirus 7 Complete Genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70
2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:BackgroundThe species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages. MethodsThe URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage. ResultsThe genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1. ConclusionsThese data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type.
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the oral cavity contains abundant known and novel human papillomaviruses from the betapapillomavirus and gammapapillomavirus genera
The Journal of Infectious Diseases, 2011Co-Authors: Danielle Bottalico, Rolando Herrero, Zigui Chen, Anne Dunne, Janae Ostoloza, Sharod Mckinney, Chang Sun, Nicolas F. Schlecht, Mahnaz Fatahzadeh, Mark SchiffmanAbstract:Human papillomaviruses (HPVs) are a heterogeneous group of closed-circular, double-stranded DNA viruses ∼8 kb in size that are established as the etiological agents of invasive cervical, anogenital, and oropharyngeal cancers [1, 2]. Currently, >140 HPV types have been fully characterized; the majority cluster into 3 genera: Alphapapillomavirus (α-HPV), predominantly isolated from genital lesions; Betapapillomavirus (β-HPV), previously referred to as Epidermodysplasia verruciformis–related types; and Gammapapillomavirus (γ-HPV). The HPV types from the latter 2 genera have been mainly isolated from skin lesions [3, 4]. It has been assumed that HPV tissue tropisms reflect the sites from which the original types were isolated. Hence, the corresponding initial sites of isolation have led to the consequent classification of α-HPVs as mucosal or genital types and β- and γ-HPVs as cutaneous types. The genital high-risk oncogenic HPV types are all members of the α-HPV genus. The tissue tropism of a group of viruses is an important biological phenotype in understanding how viruses evolve in ecological niches and induce pathogenic consequences in their hosts. Increasing evidence indicates that persistent HPV infection, particularly with certain high-risk oncogenic HPV types such as HPV type 16, is associated with some oral and/or oropharyngeal cancers [1, 5, 6]. However, previous oral HPV surveys mainly tested for α-HPV infections, possibly underestimating the overall prevalence of HPV infection in the oral cavity and in cancers of these sites [6, 7]. To evaluate the distribution of HPV in the oral cavity, we employed 2 polymerase chain reaction (PCR) systems using MY09/11 and FAP59/64 primer sets to detect α-, β-, and γ-HPV. The participants who provided oral rinse samples were part of 2 independent studies and included (1) human immunodeficiency virus (HIV)–positive men and women from an oral medicine clinic and (2) HIV-negative men of Ashkenazic descent participating in a case-control study of prostate cancer [8]. As a comparison group, a subset of cervical samples from a population-based study in Costa Rica was tested with both primer sets [9]. The HPV DNA types detected indicate that the oral cavity contains a wide spectrum of known and novel HPV types that phylogenetically cluster into the β- and γ-HPV genera, which were previously considered to be nearly exclusively skin types. The difference in the spectrum of HPV types detected in the oral cavity and exfoliated cervicovaginal cells has significant implications for our understanding of the anatomic tissue tropisms, the evolution of HPVs, and the epidemiological association of HPV with oral and skin neoplasia.
Robert D Burk - One of the best experts on this subject based on the ideXlab platform.
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Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
2018Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Charles E. Wood, Julio C. Ruiz, Gary M. Clifford, Paul K. S. Chan, Robert D BurkAbstract:Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
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RESEARCH ARTICLE Degradation of Human PDZ-Proteins by Human Alphapapillomaviruses Represents an Evolutionary Adaptation to a Novel Cellular Niche
2016Co-Authors: Koenraad Van Doorslaer, Rob Desalle, Mark H Einstein, Robert D BurkAbstract:In order to complete their life cycle, papillomaviruses have evolved to manipulate a plethora of cellular pathways. The products of the human Alphapapillomavirus E6 proteins specifi-cally interact with and target PDZ containing proteins for degradation. This viral phenotype has been suggested to play a role in viral oncogenesis. To analyze the association of HPV E6 mediated PDZ-protein degradation with cervical oncogenesis, a high-throughput cell culture assay was developed. Degradation of an epitope tagged human MAGI1 isoform was visualized by immunoblot. The correlation between HPV E6-induced degradation of hMAGI1 and epidemiologically determined HPV oncogenicity was evaluated using a Bayesian approach within a phylogenetic context. All tested oncogenic types degraded the PDZ-containing protein hMAGI1d; however, E6 proteins isolated from several related albeit non-oncogenic viral types were equally efficient at degrading hMAGI1. The relationship between both traits (oncogenicity and PDZ degradation potential) is best explained by a model in which the potential to degrade PDZ proteins was acquired prior to the oncogenic phenotype. This analysis provides evidence that the ancestor of both oncogenic and non
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degradation of human pdz proteins by human Alphapapillomaviruses represents an evolutionary adaptation to a novel cellular niche
PLOS Pathogens, 2015Co-Authors: Koenraad Van Doorslaer, Rob Desalle, Mark H Einstein, Robert D BurkAbstract:In order to complete their life cycle, papillomaviruses have evolved to manipulate a plethora of cellular pathways. The products of the human Alphapapillomavirus E6 proteins specifically interact with and target PDZ containing proteins for degradation. This viral phenotype has been suggested to play a role in viral oncogenesis. To analyze the association of HPV E6 mediated PDZ-protein degradation with cervical oncogenesis, a high-throughput cell culture assay was developed. Degradation of an epitope tagged human MAGI1 isoform was visualized by immunoblot. The correlation between HPV E6-induced degradation of hMAGI1 and epidemiologically determined HPV oncogenicity was evaluated using a Bayesian approach within a phylogenetic context. All tested oncogenic types degraded the PDZ-containing protein hMAGI1d; however, E6 proteins isolated from several related albeit non-oncogenic viral types were equally efficient at degrading hMAGI1. The relationship between both traits (oncogenicity and PDZ degradation potential) is best explained by a model in which the potential to degrade PDZ proteins was acquired prior to the oncogenic phenotype. This analysis provides evidence that the ancestor of both oncogenic and non-oncogenic HPVs acquired the potential to degrade human PDZ-containing proteins. This suggests that HPV E6 directed degradation of PDZ-proteins represents an ancient ecological niche adaptation. Phylogenetic modeling indicates that this phenotype is not specifically correlated with oncogenic risk, but may act as an enabling phenotype. The role of PDZ protein degradation in HPV fitness and oncogenesis needs to be interpreted in the context of Alphapapillomavirus evolution.
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All members of the phylogenetic high-risk clade degrade human MAGI1d.
2015Co-Authors: Koenraad Van Doorslaer, Rob Desalle, Mark H Einstein, Robert D BurkAbstract:(A) C-33A cells were transfected with 24 different E6 proteins covering the known evolutionary spectrum within the Alphapapillomavirus genus. The western blot shows a representative experiment. GFP was probed as a transfection control indicating equal transfection. This figure shows that all High-Risk types (highlighted in red) target hMAGI1d for degradation. The pQCXIN vector was used as control. (B) Mirror trees comparing the epidemiological (left) and PDZ-protein degradation (right) phenotypes on the E6 based phylogeny. The viral names are colored according to phylogenetic classification. High-risk viruses are colored in red, while LR viruses are colored green. The branches of the tree are shaded according to the state of each character under investigation.
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Degradation of PDZ proteins is an enabling phenotype towards oncogenicity.
2015Co-Authors: Koenraad Van Doorslaer, Rob Desalle, Mark H Einstein, Robert D BurkAbstract:(A) Table of top five models as selected by the RJMCMC analysis. The RJMCMC was run three independent times to ensure that the reproducibility of the model analysis. Through comparing the ratio of posterior to prior odds (see materials and methods) we obtain Bayes Factors to support the choice of a specific model. The selected model has a Bayes Factor of 130.41 (st.dev. = 1.99) suggesting decisive evidence in favor of this model. (B) Ancestral phenotype reconstruction at three important nodes of the Alphapapillomavirus phylogeny. The graphs show the estimated marginal probability density plot for the common MRCA, the high-risk MRCA or the low-risk MRCA. The analysis suggests that the MRCA of the high-risk viruses acquired the ability to degrade PDZ-containing protein, but was likely not an oncogenic virus. (C) Estimated instantaneous rates of change between different combinations of viral phenotypes based on the RJMCMC analysis. Histograms show the posterior distribution of estimated values of the rate parameters. The red bars indicate the fraction of samples in which each rate is estimated to be zero. Arrow width is proportional to the median of these estimated rates. Z indicates the percentage of samples in which each rate parameter is estimated as zero. Consistent with the hypothesis that the ability to degrade PDZ containing proteins is an enabling phenotype, rates associated with oncogenic ability independent of PDZ protein interaction are often estimated as zero (i.e. they do not occur), and are thus represented as dotted line.
Ann W Hsing - One of the best experts on this subject based on the ideXlab platform.
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evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes hpv18 hpv39 hpv45 hpv59 hpv68 and hpv70
PLOS ONE, 2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.
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Evolution and Taxonomic Classification of Alphapapillomavirus 7 Complete Genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70
2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:BackgroundThe species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages. MethodsThe URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage. ResultsThe genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1. ConclusionsThese data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type.
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evolution and taxonomic classification of human papillomavirus 16 hpv16 related variant genomes hpv31 hpv33 hpv35 hpv52 hpv58 and hpv67
PLOS ONE, 2011Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background: Human papillomavirus 16 (HPV16) species group (alpha-9) of the Alphapapillomavirus genus contains HPV16, HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67. These HPVs account for 75% of invasive cervical cancers worldwide. Viral variants of these HPVs differ in evolutionary history and pathogenicity. Moreover, a comprehensive nomenclature system for HPV variants is lacking, limiting comparisons between studies. Methods: DNA from cervical samples previously characterized for HPV type were obtained from multiple geographic regions to screen for novel variants. The complete 8 kb genomes of 120 variants representing the major and minor lineages of the HPV16-related alpha-9 HPV types were sequenced to capture maximum viral heterogeneity. Viral evolution was characterized by constructing phylogenic trees based on complete genomes using multiple algorithms. Maximal and viral region specific divergence was calculated by global and pairwise alignments. Variant lineages were classified and named using an alphanumeric system; the prototype genome was assigned to the A lineage for all types. Results: The range of genome-genome sequence heterogeneity varied from 0.6% for HPV35 to 2.2% for HPV52 and included 1.4% for HPV31, 1.1% for HPV33, 1.7% for HPV58 and 1.1% for HPV67. Nucleotide differences of approximately 1.0% - 10.0% and 0.5%–1.0% of the complete genomes were used to define variant lineages and sublineages, respectively. Each gene/region differs in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) /noncoding region 2 (NCR2) .upstream regulatory region (URR). E6/E7 . E2/L2 . E1/L1. Conclusions: These data define maximum viral genomic heterogeneity of HPV16-related alpha-9 HPV variants. The proposed nomenclature system facilitates the comparison of variants across epidemiological studies. Sequence diversity and phylogenies of this clinically important group of HPVs provides the basis for further studies of discrete viral evolution, epidemiology, pathogenesis and preventative/therapeutic interventions.
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Evolution and taxonomic classification of Human papillomavirus 16 (HPV16)-related variant genomes
2011Co-Authors: Zigui Chen, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, O Herrero, Robert D BurkAbstract:Background: Human papillomavirus 16 (HPV16) species group (alpha-9) of the Alphapapillomavirus genus contains HPV16, HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67. These HPVs account for 75 % of invasive cervical cancers worldwide. Viral variants of these HPVs differ in evolutionary history and pathogenicity. Moreover, a comprehensive nomenclature system for HPV variants is lacking, limiting comparisons between studies. Methods: DNA from cervical samples previously characterized for HPV type were obtained from multiple geographic regions to screen for novel variants. The complete 8 kb genomes of 120 variants representing the major and minor lineages of the HPV16-related alpha-9 HPV types were sequenced to capture maximum viral heterogeneity. Viral evolution was characterized by constructing phylogenic trees based on complete genomes using multiple algorithms. Maximal and vira
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Evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70.
Public Library of Science (PLoS), 2026Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.The URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage.The genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1.These data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type
Vikrant V Sahasrabuddhe - One of the best experts on this subject based on the ideXlab platform.
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evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes hpv18 hpv39 hpv45 hpv59 hpv68 and hpv70
PLOS ONE, 2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.
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Evolution and Taxonomic Classification of Alphapapillomavirus 7 Complete Genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70
2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:BackgroundThe species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages. MethodsThe URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage. ResultsThe genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1. ConclusionsThese data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type.
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evolution and taxonomic classification of human papillomavirus 16 hpv16 related variant genomes hpv31 hpv33 hpv35 hpv52 hpv58 and hpv67
PLOS ONE, 2011Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background: Human papillomavirus 16 (HPV16) species group (alpha-9) of the Alphapapillomavirus genus contains HPV16, HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67. These HPVs account for 75% of invasive cervical cancers worldwide. Viral variants of these HPVs differ in evolutionary history and pathogenicity. Moreover, a comprehensive nomenclature system for HPV variants is lacking, limiting comparisons between studies. Methods: DNA from cervical samples previously characterized for HPV type were obtained from multiple geographic regions to screen for novel variants. The complete 8 kb genomes of 120 variants representing the major and minor lineages of the HPV16-related alpha-9 HPV types were sequenced to capture maximum viral heterogeneity. Viral evolution was characterized by constructing phylogenic trees based on complete genomes using multiple algorithms. Maximal and viral region specific divergence was calculated by global and pairwise alignments. Variant lineages were classified and named using an alphanumeric system; the prototype genome was assigned to the A lineage for all types. Results: The range of genome-genome sequence heterogeneity varied from 0.6% for HPV35 to 2.2% for HPV52 and included 1.4% for HPV31, 1.1% for HPV33, 1.7% for HPV58 and 1.1% for HPV67. Nucleotide differences of approximately 1.0% - 10.0% and 0.5%–1.0% of the complete genomes were used to define variant lineages and sublineages, respectively. Each gene/region differs in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) /noncoding region 2 (NCR2) .upstream regulatory region (URR). E6/E7 . E2/L2 . E1/L1. Conclusions: These data define maximum viral genomic heterogeneity of HPV16-related alpha-9 HPV variants. The proposed nomenclature system facilitates the comparison of variants across epidemiological studies. Sequence diversity and phylogenies of this clinically important group of HPVs provides the basis for further studies of discrete viral evolution, epidemiology, pathogenesis and preventative/therapeutic interventions.
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Evolution and taxonomic classification of Human papillomavirus 16 (HPV16)-related variant genomes
2011Co-Authors: Zigui Chen, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, O Herrero, Robert D BurkAbstract:Background: Human papillomavirus 16 (HPV16) species group (alpha-9) of the Alphapapillomavirus genus contains HPV16, HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67. These HPVs account for 75 % of invasive cervical cancers worldwide. Viral variants of these HPVs differ in evolutionary history and pathogenicity. Moreover, a comprehensive nomenclature system for HPV variants is lacking, limiting comparisons between studies. Methods: DNA from cervical samples previously characterized for HPV type were obtained from multiple geographic regions to screen for novel variants. The complete 8 kb genomes of 120 variants representing the major and minor lineages of the HPV16-related alpha-9 HPV types were sequenced to capture maximum viral heterogeneity. Viral evolution was characterized by constructing phylogenic trees based on complete genomes using multiple algorithms. Maximal and vira
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Evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70.
Public Library of Science (PLoS), 2026Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.The URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage.The genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1.These data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type
Mark Schiffman - One of the best experts on this subject based on the ideXlab platform.
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Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
2018Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Charles E. Wood, Julio C. Ruiz, Gary M. Clifford, Paul K. S. Chan, Robert D BurkAbstract:Divergence time estimation of Alphapapillomavirus and Dyoomikronpapillomavirus types.
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evolution and taxonomic classification of Alphapapillomavirus 7 complete genomes hpv18 hpv39 hpv45 hpv59 hpv68 and hpv70
PLOS ONE, 2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background The species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages.
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Evolution and Taxonomic Classification of Alphapapillomavirus 7 Complete Genomes: HPV18, HPV39, HPV45, HPV59, HPV68 and HPV70
2013Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W Hsing, Robert D BurkAbstract:BackgroundThe species Alphapapillomavirus 7 (alpha-7) contains human papillomavirus genotypes that account for 15% of invasive cervical cancers and are disproportionately associated with adenocarcinoma of the cervix. Complete genome analyses enable identification and nomenclature of variant lineages and sublineages. MethodsThe URR/E6 region was sequenced to screen for novel variants of HPV18, 39, 45, 59, 68, 70, 85 and 97 from 1147 cervical samples obtained from multiple geographic regions that had previously been shown to contain an alpha-7 HPV isolate. To study viral heterogeneity, the complete 8 kb genome of 128 isolates, including 109 sequenced for this analysis, were annotated and analyzed. Viral evolution was characterized by constructing phylogenic trees using maximum-likelihood and Bayesian algorithms. Global and pairwise alignments were used to calculate total and ORF/region nucleotide differences; lineages and sublineages were assigned using an alphanumeric system. The prototype genome was assigned to the A lineage or A1 sublineage. ResultsThe genomic diversity of alpha-7 HPV types ranged from 1.1% to 6.7% nucleotide sequence differences; the extent of genome-genome pairwise intratype heterogeneity was 1.1% for HPV39, 1.3% for HPV59, 1.5% for HPV45, 1.6% for HPV70, 2.1% for HPV18, and 6.7% for HPV68. ME180 (previously a subtype of HPV68) was designated as the representative genome for HPV68 sublineage C1. Each ORF/region differed in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) / noncoding region 2 (NCR2) > upstream regulatory region (URR) > E6 / E7 > E2 / L2 > E1 / L1. ConclusionsThese data provide estimates of the maximum viral genomic heterogeneity of alpha-7 HPV type variants. The proposed taxonomic system facilitates the comparison of variants across epidemiological and molecular studies. Sequence diversity, geographic distribution and phylogenetic topology of this clinically important group of HPVs suggest an independent evolutionary history for each type.
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the oral cavity contains abundant known and novel human papillomaviruses from the betapapillomavirus and gammapapillomavirus genera
The Journal of Infectious Diseases, 2011Co-Authors: Danielle Bottalico, Rolando Herrero, Zigui Chen, Anne Dunne, Janae Ostoloza, Sharod Mckinney, Chang Sun, Nicolas F. Schlecht, Mahnaz Fatahzadeh, Mark SchiffmanAbstract:Human papillomaviruses (HPVs) are a heterogeneous group of closed-circular, double-stranded DNA viruses ∼8 kb in size that are established as the etiological agents of invasive cervical, anogenital, and oropharyngeal cancers [1, 2]. Currently, >140 HPV types have been fully characterized; the majority cluster into 3 genera: Alphapapillomavirus (α-HPV), predominantly isolated from genital lesions; Betapapillomavirus (β-HPV), previously referred to as Epidermodysplasia verruciformis–related types; and Gammapapillomavirus (γ-HPV). The HPV types from the latter 2 genera have been mainly isolated from skin lesions [3, 4]. It has been assumed that HPV tissue tropisms reflect the sites from which the original types were isolated. Hence, the corresponding initial sites of isolation have led to the consequent classification of α-HPVs as mucosal or genital types and β- and γ-HPVs as cutaneous types. The genital high-risk oncogenic HPV types are all members of the α-HPV genus. The tissue tropism of a group of viruses is an important biological phenotype in understanding how viruses evolve in ecological niches and induce pathogenic consequences in their hosts. Increasing evidence indicates that persistent HPV infection, particularly with certain high-risk oncogenic HPV types such as HPV type 16, is associated with some oral and/or oropharyngeal cancers [1, 5, 6]. However, previous oral HPV surveys mainly tested for α-HPV infections, possibly underestimating the overall prevalence of HPV infection in the oral cavity and in cancers of these sites [6, 7]. To evaluate the distribution of HPV in the oral cavity, we employed 2 polymerase chain reaction (PCR) systems using MY09/11 and FAP59/64 primer sets to detect α-, β-, and γ-HPV. The participants who provided oral rinse samples were part of 2 independent studies and included (1) human immunodeficiency virus (HIV)–positive men and women from an oral medicine clinic and (2) HIV-negative men of Ashkenazic descent participating in a case-control study of prostate cancer [8]. As a comparison group, a subset of cervical samples from a population-based study in Costa Rica was tested with both primer sets [9]. The HPV DNA types detected indicate that the oral cavity contains a wide spectrum of known and novel HPV types that phylogenetically cluster into the β- and γ-HPV genera, which were previously considered to be nearly exclusively skin types. The difference in the spectrum of HPV types detected in the oral cavity and exfoliated cervicovaginal cells has significant implications for our understanding of the anatomic tissue tropisms, the evolution of HPVs, and the epidemiological association of HPV with oral and skin neoplasia.
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evolution and taxonomic classification of human papillomavirus 16 hpv16 related variant genomes hpv31 hpv33 hpv35 hpv52 hpv58 and hpv67
PLOS ONE, 2011Co-Authors: Zigui Chen, Rolando Herrero, Mark Schiffman, Rob Desalle, Kathryn Anastos, Michel Segondy, Vikrant V Sahasrabuddhe, Patti E Gravitt, Ann W HsingAbstract:Background: Human papillomavirus 16 (HPV16) species group (alpha-9) of the Alphapapillomavirus genus contains HPV16, HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67. These HPVs account for 75% of invasive cervical cancers worldwide. Viral variants of these HPVs differ in evolutionary history and pathogenicity. Moreover, a comprehensive nomenclature system for HPV variants is lacking, limiting comparisons between studies. Methods: DNA from cervical samples previously characterized for HPV type were obtained from multiple geographic regions to screen for novel variants. The complete 8 kb genomes of 120 variants representing the major and minor lineages of the HPV16-related alpha-9 HPV types were sequenced to capture maximum viral heterogeneity. Viral evolution was characterized by constructing phylogenic trees based on complete genomes using multiple algorithms. Maximal and viral region specific divergence was calculated by global and pairwise alignments. Variant lineages were classified and named using an alphanumeric system; the prototype genome was assigned to the A lineage for all types. Results: The range of genome-genome sequence heterogeneity varied from 0.6% for HPV35 to 2.2% for HPV52 and included 1.4% for HPV31, 1.1% for HPV33, 1.7% for HPV58 and 1.1% for HPV67. Nucleotide differences of approximately 1.0% - 10.0% and 0.5%–1.0% of the complete genomes were used to define variant lineages and sublineages, respectively. Each gene/region differs in sequence diversity, from most variable to least variable: noncoding region 1 (NCR1) /noncoding region 2 (NCR2) .upstream regulatory region (URR). E6/E7 . E2/L2 . E1/L1. Conclusions: These data define maximum viral genomic heterogeneity of HPV16-related alpha-9 HPV variants. The proposed nomenclature system facilitates the comparison of variants across epidemiological studies. Sequence diversity and phylogenies of this clinically important group of HPVs provides the basis for further studies of discrete viral evolution, epidemiology, pathogenesis and preventative/therapeutic interventions.