Evidence map›Paper›PMID 28288568›Full record

ArticleBMC genomics2017

Deep sequencing of HPV E6/E7 genes reveals loss of genotypic diversity and gain of clonal dominance in high-grade intraepithelial lesions of the cervix.

Jane Shen-Gunther, Yufeng Wang, Zhao Lai, Graham M Poage, Luis Perez, Tim H M Huang

Abstract read
In one paragraph

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

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  15. The vaginal eukaryotic DNA virome and preterm birth.American journal of obstetrics and gynecology · 2018
    Article
  16. Intra-host sequence variability in human papillomavirus.Papillomavirus research (Amsterdam, Netherlands) · 2018
    Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Jane Shen-GuntherDepartment of Clinical Investigation, Brooke Army Medical Center, Gynecologic Oncology & Clinical Investigation, 3698 Chambers Pass, Fort Sam Houston, TX, 78234, USA. jane.shengunther.mil@mail.mil.ORCID 0000-0002-0876-9338
Yufeng WangDepartment of Biology, University of Texas at San Antonio, San Antonio, TX, 78249, USA.
Zhao LaiGreehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
Graham M PoageDepartment of Clinical Investigation, Brooke Army Medical Center, Gynecologic Oncology & Clinical Investigation, 3698 Chambers Pass, Fort Sam Houston, TX, 78234, USA.
Luis PerezDepartment of Clinical Investigation, Brooke Army Medical Center, Gynecologic Oncology & Clinical Investigation, 3698 Chambers Pass, Fort Sam Houston, TX, 78234, USA.
Tim H M HuangDepartment of Molecular Medicine, Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.

Funding

Systems Biology of Plasmodium falciparum: Building and Exploring Network ModelsSC1GM100806 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI WANG, YUFENG · 2012 to 2015
$1.5M
NIGMS NIH HHS SC1 GM100806
6 · The paper itself

Abstract

backgroundHuman papillomavirus (HPV) is the carcinogen of almost all invasive cervical cancer and a major cause of oral and other anogenital malignancies. HPV genotyping by dideoxy (Sanger) sequencing is currently the reference method of choice for clinical diagnostics. However, for samples with multiple HPV infections, genotype identification is singular and occasionally imprecise or indeterminable due to overlapping chromatograms. Our aim was to explore and compare HPV metagenomes in abnormal cervical cytology by deep sequencing for correlation with disease states.

resultsLow- and high-grade intraepithelial lesion (LSIL and HSIL) cytology samples were DNA extracted for PCR-amplification of the HPV E6/E7 genes. HPV+ samples were sequenced by dideoxy and deep methods. Deep sequencing revealed ~60% of all samples (n = 72) were multi-HPV infected. Among LSIL samples (n = 43), 27 different genotypes were found. The 3 dominant (most abundant) genotypes were: HPV-39, 11/43 (26%); -16, 9/43 (21%); and -35, 4/43 (9%). Among HSIL (n = 29), 17 HPV genotypes were identified; the 3 dominant genotypes were: HPV-16, 21/29 (72%); -35, 4/29 (14%); and -39, 3/29 (10%). Phylogenetically, type-specific E6/E7 genetic distances correlated with carcinogenic potential. Species diversity analysis between LSIL and HSIL revealed loss of HPV diversity and domination by HPV-16 in HSIL samples.

conclusionsDeep sequencing resolves HPV genotype composition within multi-infected cervical cytology. Biodiversity analysis reveals loss of diversity and gain of dominance by carcinogenic genotypes in high-grade cytology. Metagenomic profiles may therefore serve as a biomarker of disease severity and a population surveillance tool for emerging genotypes.

Indexed as

Base SequenceDNA, ViralEvolution, MolecularFemaleGenetic LociGenotypeHigh-Throughput Nucleotide SequencingHumansNeoplasm GradingOncogene Proteins, ViralPapillomaviridaePapillomavirus E7 ProteinsPhylogenySequence Analysis, DNAUterine Cervical NeoplasmsDNA, ViralOncogene Proteins, ViralPapillomavirus E7 ProteinsDeep sequencingHigh-throughput sequencingHPV genotypingHSILHuman papillomavirusLSILMetagenomeVirome

Identifiers

PMID28288568
PMCPMC5348809

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.