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Papillomavirus Research (Amsterdam,... Dec 2016Cervical cancer is initiated by high-risk types of the human papillomavirus (hrHPV) and develops via precursor stages, called cervical intraepithelial neoplasia (CIN).... (Review)
Review
Cervical cancer is initiated by high-risk types of the human papillomavirus (hrHPV) and develops via precursor stages, called cervical intraepithelial neoplasia (CIN). High-grade CIN lesions are considered true precancerous lesions when the viral oncogenes E6 and E7 are aberrantly expressed in the dividing cells. This results in abolishment of normal cell cycle control via p53 and pRb degradation. However, it has become clear that these viral oncogenes possess additional oncogenic properties, including interference with the DNA methylation machinery and mitotic checkpoints. Identification of the resulting molecular events leading to high-grade neoplasia will 1) increase our understanding of cervical carcinogenesis, 2) yield biomarkers for early diagnosis, and 3) identify therapeutic targets for HPV-induced (pre) cancerous lesions. This review will briefly summarise current advances in our understanding of the molecular alterations in the host cell genome that occur during HPV-induced carcinogenesis.
Topics: Carcinogenesis; Host-Pathogen Interactions; Humans; Neoplasms; Oncogene Proteins, Viral; Papillomaviridae; Papillomavirus Infections
PubMed: 29074190
DOI: 10.1016/j.pvr.2016.04.003 -
Virology Oct 2013Acceptance of an official classification for the family Papillomaviridae based purely on DNA sequence relatedness, was achieved as late as 2003. The rate of isolation... (Review)
Review
Acceptance of an official classification for the family Papillomaviridae based purely on DNA sequence relatedness, was achieved as late as 2003. The rate of isolation and characterization of new papillomavirus types has greatly depended on and subjected to the development of new laboratory techniques. Introduction of every new technique led to a temporarily burst in the number of new isolates. In the following, the bumpy road towards achieving a classification system combined with the controversies of implementing and accepting new techniques will be summarized. An update of the classification of the 170 human papillomavirus (HPV) types presently known is presented. Arguments towards the implementation of metagenomic sequencing for this rapidly growing family will be presented.
Topics: Animals; Base Sequence; DNA, Viral; Genome, Viral; Humans; Likelihood Functions; Metagenomics; Open Reading Frames; Papillomaviridae; Phylogeny
PubMed: 23683837
DOI: 10.1016/j.virol.2013.04.023 -
Advances in Virus Research 2008Papillomaviruses establish persistent infection in the dividing, basal epithelial cells of the host. The viral genome is maintained as a circular, double-stranded DNA,... (Review)
Review
Papillomaviruses establish persistent infection in the dividing, basal epithelial cells of the host. The viral genome is maintained as a circular, double-stranded DNA, extrachromosomal element within these cells. Viral genome amplification occurs only when the epithelial cells differentiate and viral particles are shed in squames that are sloughed from the surface of the epithelium. There are three modes of replication in the papillomavirus life cycle. Upon entry, in the establishment phase, the viral genome is amplified to a low copy number. In the second maintenance phase, the genome replicates in dividing cells at a constant copy number, in synchrony with the cellular DNA. And finally, in the vegetative or productive phase, the viral DNA is amplified to a high copy number in differentiated cells and is destined to be packaged in viral capsids. This review discusses the cis elements and protein factors required for each stage of papillomavirus replication.
Topics: DNA Replication; DNA, Viral; Genome, Viral; Papillomaviridae; Virus Replication
PubMed: 19081491
DOI: 10.1016/S0065-3527(08)00404-1 -
Journal of Virology Oct 2016The human papillomavirus (HPV) life cycle is tightly linked to differentiation of the infected epithelium. This means that viral proteins must exert control over... (Review)
Review
The human papillomavirus (HPV) life cycle is tightly linked to differentiation of the infected epithelium. This means that viral proteins must exert control over epithelial gene expression in order to optimize viral production. The HPV E2 protein controls replication, transcription, and viral genome partitioning during the viral infectious life cycle. It consists of a nucleic acid-binding domain and a protein-protein interaction domain separated by a flexible serine and arginine-rich hinge region. Over the last few years, mounting evidence has uncovered an important new role for E2 in viral and cellular RNA processing. This Gem discusses the role of E2 in controlling the epithelial cellular environment and how E2 might act to coordinate late events in the viral replication cycle.
Topics: Epithelial Cells; Humans; Papillomaviridae; RNA Processing, Post-Transcriptional; Transcription, Genetic; Viral Proteins; Virus Replication
PubMed: 27412596
DOI: 10.1128/JVI.00502-16 -
Virology Oct 2013Viruses belonging to the Papillomaviridae family have been isolated from a variety of mammals, birds and non-avian reptiles. It is likely that most, if not all, amniotes... (Review)
Review
Viruses belonging to the Papillomaviridae family have been isolated from a variety of mammals, birds and non-avian reptiles. It is likely that most, if not all, amniotes carry a broad array of viral types. To date, the complete genomic sequence of more than 240 distinct viral types has been characterized at the nucleotide level. The analysis of this sequence information has begun to shed light on the evolutionary history of this important virus family. The available data suggests that many different evolutionary mechanisms have influenced the papillomavirus phylogenetic tree. Increasing evidence supports that the ancestral papillomavirus initially specialized to infect different ecological niches on the host. This episode of niche sorting was followed by extensive episodes of co-speciation with the host. This review attempts to summarize our current understanding of the papillomavirus evolution.
Topics: Adaptation, Biological; Animals; Evolution, Molecular; Genetic Speciation; Host-Pathogen Interactions; Humans; Oncogene Proteins, Viral; Open Reading Frames; Papillomaviridae; Phylogeny; Repressor Proteins; Selection, Genetic; Viral Proteins
PubMed: 23769415
DOI: 10.1016/j.virol.2013.05.012 -
Viruses Sep 2021Papillomavirus L1 and L2, the major and minor capsid proteins, play significant roles in viral assembly, entry, and propagation. In the current study, we investigate the...
Papillomavirus L1 and L2, the major and minor capsid proteins, play significant roles in viral assembly, entry, and propagation. In the current study, we investigate the impact of L1 and L2 on viral life cycle and tumor growth with a newly established mouse papillomavirus (MmuPV1) infection model. MmuPV1 L1 knockout, L2 knockout, and L1 plus L2 knockout mutant genomes (designated as L1ATGko-4m, L2ATGko, and L1-L2ATGko respectively) were generated. The mutants were examined for their ability to generate lesions in athymic nude mice. Viral activities were examined by qPCR, immunohistochemistry (IHC), in situ hybridization (ISH), and transmission electron microscopy (TEM) analyses. We demonstrated that viral DNA replication and tumor growth occurred at both cutaneous and mucosal sites infected with each of the mutants. Infections involving L1ATGko-4m, L2ATGko, and L1-L2ATGko mutant genomes generally resulted in smaller tumor sizes compared to infection with the wild type. The L1 protein was absent in L1ATGko-4m and L1-L2ATGko mutant-treated tissues, even though viral transcripts and E4 protein expression were robust. Therefore, L1 is not essential for MmuPV1-induced tumor growth, and this finding parallels our previous observations in the rabbit papillomavirus model. Very few viral particles were detected in L2ATGko mutant-infected tissues. Interestingly, the localization of L1 in lesions induced by L2ATGko was primarily cytoplasmic rather than nuclear. The findings support the hypothesis that the L2 gene influences the expression, location, transport, and assembly of the L1 protein in vivo.
Topics: Animals; Capsid Proteins; Cell Transformation, Viral; DNA, Viral; Female; Genome, Viral; Mice; Mice, Nude; Mucous Membrane; Mutation; Oncogene Proteins, Viral; Papillomaviridae; Skin; Virus Replication
PubMed: 34578405
DOI: 10.3390/v13091824 -
Viruses Aug 2015The HPV viral lifecycle is tightly linked to the host cell differentiation, causing difficulty in growing virions in culture. A system that bypasses the need for... (Review)
Review
The HPV viral lifecycle is tightly linked to the host cell differentiation, causing difficulty in growing virions in culture. A system that bypasses the need for differentiating epithelium has allowed for generation of recombinant particles, such as virus-like particles (VLPs), pseudovirions (PsV), and quasivirions (QV). Much of the research looking at the HPV life cycle, infectivity, and structure has been generated utilizing recombinant particles. While recombinant particles have proven to be invaluable, allowing for a rapid progression of the HPV field, there are some significant differences between recombinant particles and native virions and very few comparative studies using native virions to confirm results are done. This review serves to address the conflicting data in the HPV field regarding native virions and recombinant particles.
Topics: Humans; Papillomaviridae; Papillomavirus Infections; Recombination, Genetic; Virion; Virology; Virus Cultivation
PubMed: 26247955
DOI: 10.3390/v7082823 -
Papillomavirus Research (Amsterdam,... Dec 2019
Review
Topics: Animals; Clinical Trials as Topic; Combined Modality Therapy; Female; Host-Pathogen Interactions; Humans; Immunotherapy; Neoplasms; Papillomaviridae; Papillomavirus Infections; Treatment Outcome
PubMed: 31310819
DOI: 10.1016/j.pvr.2019.100176 -
The Journal of Evidence-based Dental... Dec 2020To estimate the association of human papillomavirus (HPV) infection with oral lichen planus (OLP) and oral leukoplakia (OLK), and determine risk cofactors. (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
To estimate the association of human papillomavirus (HPV) infection with oral lichen planus (OLP) and oral leukoplakia (OLK), and determine risk cofactors.
STUDY DESIGN
Seven databases were searched for case-control or cross-sectional studies of OLP and OLK with healthy controls, published between 1976 and 2020. The Meta package of R software was applied to calculate the pooled odds ratios (OR) and 95% confidence interval (CI).
RESULTS
Thirty-six articles were finally included. OLP and OLK cases had a higher association with HPV infection than controls (OLP: OR: 4.91, 95% CI: 2.76-8.72; OLK: OR: 2.51, 95% CI: 1.55-4.07). In subgroup analyses, the OR of HPV infection was higher with erosive lesions than with nonerosive lesions (OLP: OR: 5.36 and 3.47, respectively; OLK: OR: 3.34 and 3.21, respectively). Oral lesions were more strongly associated with HPV16/18 than with HPV6/11 (OLP: OR: 7.84 and 1.42, respectively; OLK: OR: 6.05 and 1.87, respectively) and varied by geographic region (OLP: OR: 4.01-7.02; OLK: OR: 1.46-27.13).
CONCLUSIONS
Oral HPV infection, particularly infection with HPV 16/18, was strongly associated with OLP and OLK. Risk cofactors included erosive lesions and geographic region.
Topics: Alphapapillomavirus; Cross-Sectional Studies; Human papillomavirus 16; Human papillomavirus 18; Humans; Leukoplakia, Oral; Lichen Planus, Oral; Papillomaviridae
PubMed: 33303094
DOI: 10.1016/j.jebdp.2020.101485 -
Viruses Aug 2017Extracellular vesicles (EVs), including exosomes (Exos), microvesicles (MVs) and apoptotic bodies (ABs) are released in biofluids by virtually all living cells.... (Review)
Review
Extracellular vesicles (EVs), including exosomes (Exos), microvesicles (MVs) and apoptotic bodies (ABs) are released in biofluids by virtually all living cells. Tumor-derived Exos and MVs are garnering increasing attention because of their ability to participate in cellular communication or transfer of bioactive molecules (mRNAs, microRNAs, DNA and proteins) between neighboring cancerous or normal cells, and to contribute to human cancer progression. Malignant traits can also be transferred from apoptotic cancer cells to phagocytizing cells, either professional or non-professional. In this review, we focus on Exos and ABs and their relationship with human papillomavirus (HPV)-associated tumor development. The potential implication of EVs as theranostic biomarkers is also addressed.
Topics: Animals; Biomarkers; Carcinogenesis; Cell Communication; Exosomes; Extracellular Vesicles; Gene Transfer, Horizontal; Humans; Mice; MicroRNAs; Neoplasms; Oncogenes; Papillomaviridae; RNA, Messenger
PubMed: 28783104
DOI: 10.3390/v9080211