Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.1
4.7
Journals
Viruses
Special Issues
HPV Genomics
share announcement

HPV Genomics

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (17 December 2021) | Viewed by 12469

Special Issue Editors

Dr. Lisa Mirabello

E-Mail Website
Guest Editor
Senior Investigator, Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 9609 Medical Center Drive, Room 6E524, Bethesda, MD 20850-9772, USA
Interests: HPV; Pediatric Cancer Genomics-Osteosarcoma; Carcinogenic HPV Genomics
Dr. Meredith Yeager

E-Mail Website
Guest Editor
Scientific Director, Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research and Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 9615 Medical Center Drive, Room 2106, Bethesda, MD 20850
Interests: HPV; HPV Genomics

Special Issue Information

Dear Colleagues, 

There are 13 carcinogenic HPV types that cause more than 600,000 cancers worldwide each year at the cervix and at non-cervical sites. We do not know why there is a large variability in risk of precancer and cancer conferred by different HPV types, or why only a small proportion of carcinogenic HPV infections progress to precancer and subsequently cancer. Sequencing the genomes of HPV specimens from large population-based studies of benign HPV infections and precancer/cancer enables the interrogation of the HPV genetic basis of carcinogenicity and is providing insights into the natural history of an HPV infection. High-throughput HPV whole-genome sequencing using next-generation sequencing technology has enabled the large-scale study of HPV genome variability. Several studies have now uncovered strong associations between HPV genetic variation and cervical carcinogenicity as well as new insights into HPV diversity in the population.

We are excited to dedicate a Special Issue of Viruses to highlight advances in our understanding of HPV genomic variation and how this relates to HPV natural history and carcinogenesis.

Sincerely,

Dr. Lisa Mirabello
Dr. Meredith Yeager
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • HPV genetic variation
  • HPV genomics
  • Carcinogenic HPV
  • HPV genetic epidemiology

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

19 pages, 2083 KiB  
Article
Phylogenomic Analysis of Human Papillomavirus Type 31 and Cervical Carcinogenesis: A Study of 2093 Viral Genomes
by Maisa Pinheiro, Ariana Harari, Mark Schiffman, Gary M. Clifford, Zigui Chen, Meredith Yeager, Michael Cullen, Joseph F. Boland, Tina Raine-Bennett, Mia Steinberg, Sara Bass, Yanzi Xiao, Vanessa Tenet, Kai Yu, Bin Zhu, Laurie Burdett, Sevilay Turan, Thomas Lorey, Philip E. Castle, Nicolas Wentzensen, Robert D. Burk and Lisa Mirabelloadd Show full author list remove Hide full author list
Viruses 2021, 13(10), 1948; https://0-doi-org.brum.beds.ac.uk/10.3390/v13101948 - 28 Sep 2021
Cited by 7 | Viewed by 2488
Abstract
Human papillomavirus (HPV) type 31 (HPV31) is closely related to the most carcinogenic type, HPV16, but only accounts for 4% of cervical cancer cases worldwide. Viral genetic and epigenetic variations have been associated with carcinogenesis for other high-risk HPV types, but little is [...] Read more.
Human papillomavirus (HPV) type 31 (HPV31) is closely related to the most carcinogenic type, HPV16, but only accounts for 4% of cervical cancer cases worldwide. Viral genetic and epigenetic variations have been associated with carcinogenesis for other high-risk HPV types, but little is known about HPV31. We sequenced 2093 HPV31 viral whole genomes from two large studies, one from the U.S. and one international. In addition, we investigated CpG methylation in a subset of 175 samples. We evaluated the association of HPV31 lineages/sublineages, single nucleotide polymorphisms (SNPs) and viral methylation with cervical carcinogenesis. HPV31 A/B clade was >1.8-fold more associated with cervical intraepithelial neoplasia grade 3 and cancer (CIN3+) compared to the most common C lineage. Lineage/sublineage distribution varied by race/ethnicity and geographic region. A viral genome-wide association analysis identified SNPs within the A/B clade associated with CIN3+, including H23Y (C626T) (odds ratio = 1.60, confidence intervals = 1.17–2.19) located in the pRb CR2 binding-site within the E7 oncogene. Viral CpG methylation was higher in lineage B, compared to the other lineages, and was most elevated in CIN3+. In conclusion, these data support the increased oncogenicity of the A/B lineages and suggest variation of E7 as a contributing risk factor. Full article
(This article belongs to the Special Issue HPV Genomics)
►▼ Show Figures

Figure 1

11 pages, 12157 KiB  
Article
APOBEC Mutagenesis Is Concordant between Tumor and Viral Genomes in HPV-Positive Head and Neck Squamous Cell Carcinoma
by Daniel L. Faden, Krystle A. Lang Kuhs, Maoxuan Lin, Adam Langenbucher, Maisa Pinheiro, Meredith Yeager, Michael Cullen, Joseph F. Boland, Mia Steinberg, Sara Bass, James S. Lewis, Michael S. Lawrence, Robert L. Ferris and Lisa Mirabello
Viruses 2021, 13(8), 1666; https://0-doi-org.brum.beds.ac.uk/10.3390/v13081666 - 23 Aug 2021
Cited by 18 | Viewed by 3479
Abstract
APOBEC is a mutagenic source in human papillomavirus (HPV)-mediated malignancies, including HPV+ oropharyngeal squamous cell carcinoma (HPV + OPSCC), and in HPV genomes. It is unknown why APOBEC mutations predominate in HPV + OPSCC, or if the APOBEC-induced mutations observed in both human [...] Read more.
APOBEC is a mutagenic source in human papillomavirus (HPV)-mediated malignancies, including HPV+ oropharyngeal squamous cell carcinoma (HPV + OPSCC), and in HPV genomes. It is unknown why APOBEC mutations predominate in HPV + OPSCC, or if the APOBEC-induced mutations observed in both human cancers and HPV genomes are directly linked. We performed sequencing of host somatic exomes, transcriptomes, and HPV16 genomes from 79 HPV + OPSCC samples, quantifying APOBEC mutational burden and activity in both host and virus. APOBEC was the dominant mutational signature in somatic exomes. In viral genomes, there was a mean of five (range 0–29) mutations per genome. The mean of APOBEC mutations in viral genomes was one (range 0–5). Viral APOBEC mutations, compared to non-APOBEC mutations, were more likely to be low-variant allele fraction mutations, suggesting that APOBEC mutagenesis actively occurrs in viral genomes during infection. HPV16 APOBEC-induced mutation patterns in OPSCC were similar to those previously observed in cervical samples. Paired host and viral analyses revealed that APOBEC-enriched tumor samples had higher viral APOBEC mutation rates (p = 0.028), and APOBEC-associated RNA editing (p = 0.008), supporting the concept that APOBEC mutagenesis in host and viral genomes is directly linked and occurrs during infection. Using paired sequencing of host somatic exomes, transcriptomes, and viral genomes, we demonstrated for the first-time definitive evidence of concordance between tumor and viral APOBEC mutagenesis. This finding provides a missing link connecting APOBEC mutagenesis in host and virus and supports a common mechanism driving APOBEC dysregulation. Full article
(This article belongs to the Special Issue HPV Genomics)
►▼ Show Figures

Figure 1

18 pages, 670 KiB  
Article
Human Papillomavirus Detection by Whole-Genome Next-Generation Sequencing: Importance of Validation and Quality Assurance Procedures
by Laila Sara Arroyo Mühr, Daniel Guerendiain, Kate Cuschieri and Karin Sundström
Viruses 2021, 13(7), 1323; https://0-doi-org.brum.beds.ac.uk/10.3390/v13071323 - 08 Jul 2021
Cited by 12 | Viewed by 3551
Abstract
Next-generation sequencing (NGS) yields powerful opportunities for studying human papillomavirus (HPV) genomics for applications in epidemiology, public health, and clinical diagnostics. HPV genotypes, variants, and point mutations can be investigated in clinical materials and described in previously unprecedented detail. However, both the NGS [...] Read more.
Next-generation sequencing (NGS) yields powerful opportunities for studying human papillomavirus (HPV) genomics for applications in epidemiology, public health, and clinical diagnostics. HPV genotypes, variants, and point mutations can be investigated in clinical materials and described in previously unprecedented detail. However, both the NGS laboratory analysis and bioinformatical approach require numerous steps and checks to ensure robust interpretation of results. Here, we provide a step-by-step review of recommendations for validation and quality assurance procedures of each step in the typical NGS workflow, with a focus on whole-genome sequencing approaches. The use of directed pilots and protocols to ensure optimization of sequencing data yield, followed by curated bioinformatical procedures, is particularly emphasized. Finally, the storage and sharing of data sets are discussed. The development of international standards for quality assurance should be a goal for the HPV NGS community, similar to what has been developed for other areas of sequencing efforts including microbiology and molecular pathology. We thus propose that it is time for NGS to be included in the global efforts on quality assurance and improvement of HPV-based testing and diagnostics. Full article
(This article belongs to the Special Issue HPV Genomics)
►▼ Show Figures

Figure 1

16 pages, 2406 KiB  
Article
Mutation Profiles, Glycosylation Site Distribution and Codon Usage Bias of Human Papillomavirus Type 16
by Wei Liu, Junhua Li, Hongli Du and Zhihua Ou
Viruses 2021, 13(7), 1281; https://0-doi-org.brum.beds.ac.uk/10.3390/v13071281 - 30 Jun 2021
Cited by 5 | Viewed by 2090
Abstract
Human papillomavirus type 16 (HPV16) is the most prevalent HPV type causing cervical cancers. Herein, using 1597 full genomes, we systemically investigated the mutation profiles, surface protein glycosylation sites and the codon usage bias (CUB) of HPV16 from different lineages and sublineages. Multiple [...] Read more.
Human papillomavirus type 16 (HPV16) is the most prevalent HPV type causing cervical cancers. Herein, using 1597 full genomes, we systemically investigated the mutation profiles, surface protein glycosylation sites and the codon usage bias (CUB) of HPV16 from different lineages and sublineages. Multiple lineage- or sublineage-conserved mutation sites were identified. Glycosylation analysis showed that HPV16 lineage D contained the highest number of different glycosylation sites from lineage A in both L1 and L2 capsid proteins, which might lead to their antigenic distances between the two lineages. CUB analysis showed that the HPV16 open reading frames (ORFs) preferred codons ending with A/T. The CUB of HPV16 ORFs was mainly affected by natural selection except for E1, E5 and L2. HPV16 only shared some of the preferred codons with humans, which might help reduce competition in translational resources. These findings increase our understanding of the heterogeneity between HPV16 lineages and sublineages, and the adaptation mechanism of HPV in human cells. In summary, this study might facilitate HPV classification and improve vaccine development and application. Full article
(This article belongs to the Special Issue HPV Genomics)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop