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1

White, Elizabeth A. "Manipulation of Epithelial Differentiation by HPV Oncoproteins." Viruses 11, no. 4 (April 22, 2019): 369. http://dx.doi.org/10.3390/v11040369.

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Papillomaviruses replicate and cause disease in stratified squamous epithelia. Epithelial differentiation is essential for the progression of papillomavirus replication, but differentiation is also impaired by papillomavirus-encoded proteins. The papillomavirus E6 and E7 oncoproteins partially inhibit and/or delay epithelial differentiation and some of the mechanisms by which they do so are beginning to be defined. This review will outline the key features of the relationship between HPV infection and differentiation and will summarize the data indicating that papillomaviruses alter epithelial differentiation. It will describe what is known so far and will highlight open questions about the differentiation-inhibitory mechanisms employed by the papillomaviruses.
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2

Torres, Sheila M. F., and Sandra N. Koch. "Papillomavirus-Associated Diseases." Veterinary Clinics of North America: Equine Practice 29, no. 3 (December 2013): 643–55. http://dx.doi.org/10.1016/j.cveq.2013.08.003.

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3

Carrai, Maura, Kate Van Brussel, Mang Shi, Ci-Xiu Li, Wei-Shan Chang, John S. Munday, Katja Voss, et al. "Identification of a Novel Papillomavirus Associated with Squamous Cell Carcinoma in a Domestic Cat." Viruses 12, no. 1 (January 20, 2020): 124. http://dx.doi.org/10.3390/v12010124.

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Papillomaviruses infect the skin and mucosal surfaces of diverse animal hosts with consequences ranging from asymptomatic colonization to highly malignant epithelial cancers. Increasing evidence suggests a role for papillomaviruses in the most common cutaneous malignancy of domestic cats, squamous cell carcinoma (SCC). Using total DNA sequencing we identified a novel feline papillomavirus in a nasal biopsy taken from a cat presenting with both nasal cavity lymphoma and recurrent squamous cell carcinoma affecting the nasal planum. We designate this novel virus as Felis catus papillomavirus 6 (FcaPV6). The complete FcaPV6 7453 bp genome was similar to those of other feline papillomaviruses and phylogenetic analysis revealed that it was most closely related to FcaPV3, although was distinct enough to represent a new viral type. Classification of FcaPV6 in a new genus alongside FcaPVs 3, 4 and 5 is supported. Archived excisional biopsy of the SCC, taken 20 months prior to presentation, was intensely positive on p16 immunostaining. FcaPV6, amplified using virus-specific, but not consensus, PCR, was the only papillomavirus detected in DNA extracted from the SCC. Conversely, renal lymphoma, sampled at necropsy two months after presentation, tested negative on FcaPV6-specific PCR. In sum, using metagenomics we demonstrate the presence of a novel feline papillomavirus in association with cutaneous squamous cell carcinoma.
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4

Knight, C. G., J. S. Munday, J. Peters, and M. Dunowska. "Equine Penile Squamous Cell Carcinomas Are Associated With the Presence of Equine Papillomavirus Type 2 DNA Sequences." Veterinary Pathology 48, no. 6 (January 31, 2011): 1190–94. http://dx.doi.org/10.1177/0300985810396516.

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Forty cases of equine penile disease were screened with polymerase chain reaction for the presence of papillomaviral DNA. Cases consisted of 20 squamous cell carcinomas (average age of horse, 23.9 years) and 20 non–squamous cell carcinoma diseases (average age of horse, 13.3 years). All horses but one originated from the Northeastern United States. Breeds were not recorded. As based on MY09/MY11 consensus primers, DNA sequences from equine papillomavirus type 2 were amplified from 9 of 20 horses (45%) with penile squamous cell carcinoma and only 1 of 20 horses (5%) with non–squamous cell carcinoma penile disease. Equine papillomavirus type 2 DNA was the only papillomaviral DNA amplified from any of the 40 horses. Tissues from the 10 horses in which papillomaviral DNA was detected by polymerase chain reaction were also screened with in situ hybridization and immunohistochemistry. The presence of papillomavirus was demonstrated in a subset of these by in situ hybridization (6 of 10) and immunohistochemistry (1 of 10). This report describes a possible association between equine penile squamous cell carcinomas and equine papillomavirus type 2. This study is also the first report of equine papillomavirus type 2 infection in North American horses.
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5

Grce, Magdalena, and Marinka Mravak-Stipetić. "Human papillomavirus–associated diseases." Clinics in Dermatology 32, no. 2 (March 2014): 253–58. http://dx.doi.org/10.1016/j.clindermatol.2013.10.006.

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6

Orth, G. "Papillomavirus." Médecine et Maladies Infectieuses 17, no. 11 (November 1987): 617. http://dx.doi.org/10.1016/s0399-077x(87)80113-0.

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7

Suzuki, Mikio, Masahiro Hasegawa, Zeyi Deng, Hiroyuki Maeda, Asanori Kiyuna, and Takayuki Uehara. "Human Papillomavirus in Sinonasal Diseases." Otolaryngology–Head and Neck Surgery 147, no. 2_suppl (August 2012): P249. http://dx.doi.org/10.1177/0194599812451426a395.

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8

Arron, Sarah Tuttleton, Peter Skewes-Cox, Phong H. Do, Eric Dybbro, Maria Da Costa, Joel M. Palefsky, and Joseph L. DeRisi. "Validation of a Diagnostic Microarray for Human Papillomavirus: Coverage of 102 Genotypes." Journal of Nucleic Acids 2011 (2011): 1–6. http://dx.doi.org/10.4061/2011/756905.

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Papillomaviruses have been implicated in a variety of human diseases ranging from common warts to invasive carcinoma of the anogenital mucosa. Existing assays for genotyping human papillomavirus are restricted to a small number of types. Here, we present a comprehensive, accurate microarray strategy for detection and genotyping of 102 human papillomavirus types and validate its use in a panel of 91 anal swabs. This array has equal performance to traditional dot blot analysis with the benefits of added genotype coverage and the ability to calibrate readout over a range of sensitivity or specificity values.
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9

Hartmann, Samantha R., Daniel J. Goetschius, Jiafen Hu, Joshua J. Graff, Carol M. Bator, Neil D. Christensen, and Susan L. Hafenstein. "Cryo EM Analysis Reveals Inherent Flexibility of Authentic Murine Papillomavirus Capsids." Viruses 13, no. 10 (October 7, 2021): 2023. http://dx.doi.org/10.3390/v13102023.

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Human papillomavirus (HPV) is a significant health burden and leading cause of virus-induced cancers. However, studies have been hampered due to restricted tropism that makes production and purification of high titer virus problematic. This issue has been overcome by developing alternative HPV production methods such as virus-like particles (VLPs), which are devoid of a native viral genome. Structural studies have been limited in resolution due to the heterogeneity, fragility, and stability of the VLP capsids. The mouse papillomavirus (MmuPV1) presented here has provided the opportunity to study a native papillomavirus in the context of a common laboratory animal. Using cryo EM to solve the structure of MmuPV1, we achieved 3.3 Å resolution with a local symmetry refinement method that defined smaller, symmetry related subparticles. The resulting high-resolution structure allowed us to build the MmuPV1 asymmetric unit for the first time and identify putative L2 density. We also used our program ISECC to quantify capsid flexibility, which revealed that capsomers move as rigid bodies connected by flexible linkers. The MmuPV1 flexibility was comparable to that of a HPV VLP previously characterized. The resulting MmuPV1 structure is a promising step forward in the study of papillomavirus and will provide a framework for continuing biochemical, genetic, and biophysical research for papillomaviruses.
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10

Zarochentseva, N. V., V. I. Krasnopolskiy, О. А. Misyukevich, I. V. Barinova, М. V. Mgeliashvili, and О. V. Rovinskaya. "Rare forms of vaginal diseases in women after panhysterectomy." Voprosy ginekologii, akušerstva i perinatologii 19, no. 5 (2020): 150–55. http://dx.doi.org/10.20953/1726-1678-2020-5-150-155.

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The article presents clinical observations of the development of precancerous conditions of the vaginal vault, and also squamous cell cancer in women after panhysterectomy. The examination included: comprehensive vaginoscopy, cytological examination of vaginal wall smears, human papillomavirus test, histological examination of bioplates. Conclusion. Panhysterectomy does not guarantee the absence of precancerous lesions of the vagina or vaginal cancer. Therefore, routine screening (cytology, testing for high-risk human papillomavirus, vaginoscopy) should be continued in women after panhysterectomy with a history of cervical intraepithelial neoplasias for at least 20 years, even in women older than 65 years. Key words: vaginal intraepithelial neoplasia, human papillomavirus, panhysterectomy, papillomavirus infection, cervical cancer, photodynamic therapy
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11

Gunder, Laura C., Simon Blaine-Sauer, Hillary R. Johnson, Myeong-Kyun Shin, Andrew S. Auyeung, Wei Zhang, Glen E. Leverson, et al. "Efficacy of Topically Administered Dihydroartemisinin in Treating Papillomavirus-Induced Anogenital Dysplasia in Preclinical Mouse Models." Viruses 14, no. 8 (July 26, 2022): 1632. http://dx.doi.org/10.3390/v14081632.

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The artemisinin family of compounds is cytopathic in certain cancer cell lines that are positive for human papillomaviruses (HPV) and can potentially drive the regression of dysplastic lesions. We evaluated the efficacy of topical dihydroartemisinin (DHA) on cervical dysplasia and anal dysplasia in two papillomavirus mouse models: K14E6/E7 transgenic mice, which express HPV16 oncogenes; and immunodeficient NOD/SCID gamma (NSG) mice infected with Mus musculus papillomavirus (MmuPV1). Mice started treatment with DHA at 25 weeks of age (K14E6/E7) or 20 weeks post infection (MmuPV1-infected), when the majority of mice are known to have papillomavirus-induced low- to high-grade dysplasia. Mice were treated with or without topical DHA at the cervix or anus and with or without topical treatment with the chemical carcinogen 7,12 dimethylbenz(a)anthracene (DMBA) at the anus of in transgenic mice to induce neoplastic progression. Mice were monitored for overt tumor growth, and tissue was harvested after 20 weeks of treatment and scored for severity of histological disease. For MmuPV1-infected mice, anogenital lavages were taken to monitor for viral clearance. Tissues were also evaluated for viral gene expression at the RNA and/or protein levels. Treatment with topical DHA did not reduce dysplasia in the anogenital tract in either papillomavirus-induced mouse model and did not prevent progression to anal cancer in the DMBA-treated K14E6/E7 mice.
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12

Prowse, David. "Papillomavirus research." Lancet Infectious Diseases 6, no. 4 (April 2006): 198. http://dx.doi.org/10.1016/s1473-3099(06)70432-7.

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13

Sichero, Laura, Dana E. Rollison, Rossybelle P. Amorrortu, and Massimo Tommasino. "Beta Human Papillomavirus and Associated Diseases." Acta Cytologica 63, no. 2 (2019): 100–108. http://dx.doi.org/10.1159/000492659.

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The cutaneous human papillomavirus (HPV), mostly from β- and γ-HPV genus, is ubiquitously distributed throughout the human body and may be part of the commensal flora. The association of β-HPVs and cutaneous squamous cell carcinoma (cSCC) development was initially reported in patients with the rare genetic disorder Epidermodysplasia verruciformis. Likewise, immunosuppressed organ transplant recipients have an increased susceptibility to β-HPV infections in the skin as well as to cSCC development. Although ultraviolet radiation (UVR) is the main risk factor of cSCC, experimental data points toward β-HPVs as co-carcinogens, which appear to be required solely at early stages of skin carcinogenesis by facilitating the accumulation of UVR-induced DNA mutations. Several epidemiological studies relying on different biomarkers of β-HPV infections have also been conducted in immunocompetent individuals to access their association with cSCC development. Additionally, in vivo and in vitro studies are presenting cumulative evidence that E6 and E7 proteins from specific β-HPVs exhibit transforming activities and may collaborate with different environmental factors in promoting carcinogenesis. Nevertheless, further research is crucial to better understand the pathological implications of the broad distribution of these HPVs.
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14

Nasir, Lubna, and Sabine Brandt. "Papillomavirus associated diseases of the horse." Veterinary Microbiology 167, no. 1-2 (November 2013): 159–67. http://dx.doi.org/10.1016/j.vetmic.2013.08.003.

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15

Cubie, Heather A. "Diseases associated with human papillomavirus infection." Virology 445, no. 1-2 (October 2013): 21–34. http://dx.doi.org/10.1016/j.virol.2013.06.007.

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16

Quinlan, Sarah, Susan May, Ryan Weeks, Hang Yuan, and Jennifer A. Luff. "Abrogation of Constitutive and Induced Type I and Type III Interferons and Interferon-Stimulated Genes in Keratinocytes by Canine Papillomavirus 2 E6 and E7." Viruses 12, no. 6 (June 23, 2020): 677. http://dx.doi.org/10.3390/v12060677.

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Cutaneous papillomaviruses can cause severe, persistent infections and skin cancer in immunodeficient patients, including people with X-linked severe combined immunodeficiency (XSCID). A similar phenotype is observed in a canine model of XSCID; these dogs acquire severe cutaneous papillomavirus infections that can progress to cancer in association with canine papillomavirus type 2 (CPV2). This canine model system provides a natural spontaneous animal model for investigation of papillomavirus infections in immunodeficient patients. Currently, it is unknown if CPV2 can subvert the innate immune system and interfere with its ability to express antiviral cytokines, which are critical in the host defense against viral pathogens. The aim of the current study was to determine if the oncogenes E6 and E7 from CPV2 interfere with expression of antiviral cytokines in keratinocytes, the target cells of papillomavirus infections. We determined that E6 but not E7 interferes with the constitutive expression of some antiviral cytokines, including interferon (IFN)-β and the IFN-stimulated gene IFIT1. Both E6 and E7 interfere with the transcriptional upregulation of the antiviral cytokines in response to stimulation with the dsDNA Poly(dA:dT). In contrast, while E6 also interferes with the transcriptional upregulation of antiviral cytokines in response to stimulation with the dsRNA Poly(I:C), E7 interferes with only a subset of these antiviral cytokines. Finally, we demonstrated that E7 but not E6 abrogates signaling through the type I IFN receptor. Taken together, CPV2 E6 and E7 both impact expression of antiviral cytokines in canine keratinocytes, albeit likely through different mechanisms.
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17

Moreno, Ruben, Darya Buehler, and Paul F. Lambert. "MmuPV1-Induced Cutaneous Squamous Cell Carcinoma Arises Preferentially from Lgr5+ Epithelial Progenitor Cells." Viruses 14, no. 8 (August 11, 2022): 1751. http://dx.doi.org/10.3390/v14081751.

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Murine papillomavirus, MmuPV1, causes natural infections in laboratory mice that can progress to squamous cell carcinoma (SCC) making it a useful preclinical model to study the role of papillomaviruses in cancer. Papillomavirus can infect cells within hair follicles, which contain multiple epithelial progenitor cell populations, including Lgr5+ progenitors, and transgenic mice expressing human papillomavirus oncogenes develop tumors derived from Lgr5 progenitors. We therefore tested the hypothesis that Lgr5+ progenitors contribute to neoplastic lesions arising in skins infected with MmuPV1 by performing lineage tracing experiments. Ears of 6–8-week-old Lgr5-eGFP-IRES-CreERT2/Rosa26LSLtdTomato mice were treated topically with 4-OH Tamoxifen to label Lgr5+ progenitor cells and their progeny with tdTomato and, 72 h later, infected with MmuPV1. Four months post-infection, tissue at the infection site was harvested for histopathological analysis and immunofluorescence to determine the percentage of tdTomato+ cells within the epithelial lesions caused by MmuPV1. Squamous cell dysplasia showed a low percentage of tdTomato+ cells (7%), indicating that it arises primarily from non-Lgr5 progenitor cells. In contrast, cutaneous SCC (cSCC) was substantially more positive for tdTomato+ cells (42%), indicating that cSCCs preferentially arise from Lgr5+ progenitors. Biomarker analyses of dysplasia vs. cSCC revealed further differences consistent with cSCC arising from LGR5+ progenitor cells.
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18

Van Doorslaer, Koenraad. "Revisiting Papillomavirus Taxonomy: A Proposal for Updating the Current Classification in Line with Evolutionary Evidence." Viruses 14, no. 10 (October 21, 2022): 2308. http://dx.doi.org/10.3390/v14102308.

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Papillomaviruses infect a wide array of animal hosts and are responsible for roughly 5% of all human cancers. Comparative genomics between different virus types belonging to specific taxonomic groupings (e.g., species, and genera) has the potential to illuminate physiological differences between viruses with different biological outcomes. Likewise, extrapolation of features between related viruses can be very powerful but requires a solid foundation supporting the evolutionary relationships between viruses. The current papillomavirus classification system is based on pairwise sequence identity. However, with the advent of metagenomics as facilitated by high-throughput sequencing and molecular tools of enriching circular DNA molecules using rolling circle amplification, there has been a dramatic increase in the described diversity of this viral family. Not surprisingly, this resulted in a dramatic increase in absolute number of viral types (i.e., sequences sharing <90% L1 gene pairwise identity). Many of these novel viruses are the sole member of a novel species within a novel genus (i.e., singletons), highlighting that we have only scratched the surface of papillomavirus diversity. I will discuss how this increase in observed sequence diversity complicates papillomavirus classification. I will propose a potential solution to these issues by explicitly basing the species and genera classification on the evolutionary history of these viruses based on the core viral proteins (E1, E2, and L1) of papillomaviruses. This strategy means that it is possible that a virus identified as the closest neighbor based on the E1, E2, L1 phylogenetic tree, is not the closest neighbor based on L1 nucleotide identity. In this case, I propose that a virus would be considered a novel type if it shares less than 90% identity with its closest neighbors in the E1, E2, L1 phylogenetic tree.
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19

Stanley, MA, PJ Masterson, and PK Nicholls. "In vitro and Animal Models for Antiviral Therapy in Papillomavirus Infections." Antiviral Chemistry and Chemotherapy 8, no. 5 (October 1997): 381–400. http://dx.doi.org/10.1177/095632029700800501.

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The need for antiviral therapies for papillomavirus infections is well recognized but the difficulties of reproducing the infectious cycle of papillomaviruses in vitro has hindered our understanding of virus-cell interactions and the regulation of viral gene expression during permissive growth. Recent advances in understanding the temporal expression and function of papillomavirus proteins has enabled consideration of a targeted approach to papillomavirus chemotherapy and in particular the inhibition of viral replication by targeting the E1 and E2 proteins. There are in vitro culture systems available for the screening of new chemotherapeutic agents, since significant advances have been made with culture systems which promote epithelial differentiation in vitro. However, to date, there are no published data which show that virions generated in vitro can infect keratinocytes and initiate another round of replication in vitro. In vivo animal models are therefore necessary to assess the efficacy of antivirals in preventing and treating viral infection, particularly for the low-risk genital viruses which are on the whole refractory to culture in vitro. Although papillomaviruses affect a wide variety of hosts in a species-specific manner, the animals most useful for modelling papillomavirus infections include the rabbit, ox, mouse, dog, horse, primate and sheep. The ideal animal model should be widely available, easy to house and handle, be large enough to allow for adequate tissue sampling, develop lesions on anatomical sites comparable with those in human diseases and these lesions should be readily accessible for monitoring and ideally should yield large amounts of infectious virus particles for use in both in vivo and in vitro studies. The relative merits of the various papillomavirus animal models available in relation to these criteria are discussed.
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20

Bősze, Péter. "The first vaccine against cancer: the human papillomavirus vaccine." Orvosi Hetilap 154, no. 16 (April 2013): 603–18. http://dx.doi.org/10.1556/oh.2013.29593.

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The last 20 years is one of the most remarkable periods in the fight against cancer, with the realization that some human papillomaviruses are causally related to cancer and with the development of the vaccine against human papillomavirus infections. This is a historical event in medicine and the prophylactic human papillomavirus vaccines have provided powerful tools for primary prevention of cervical cancer and other human papillomavirus-associated diseases. This is very important as human papillomavirus infection is probably the most common sexually transmitted infection worldwide, and over one million women develop associated cancer yearly, which is about 5% of all female cancers, and half of them die of their disease. Cancers associated with oncogenic human papillomaviruses, mostly HPV16 and 18, include cervical cancer (100%), anal cancer (95%), vulvar cancer (40%), vaginal cancer (60%), penile cancer (40%), and oro-pharingeal cancers (65%). In addition, pre-cancers such as genital warts and the rare recurrent respiratory papillomatosis are also preventable by vaccination. Currently, the human papillomavirus vaccines have the potential to significantly reduce the burden of human papillomavirus associated conditions, including prevention of up to 70% of cervical cancers. Two prophylactic human papillomavirus vaccines are currently available worldwide: a bivalent vaccine (types 16 and 18), and a quadrivalent vaccine (types 6, 11, 16, and 18). Randomized controlled trials conducted on several continents during the last 10 years have demonstrated that these vaccines are safe without serious side effects; they are highly immunogenic and efficacious in preventing incident and persistent vaccine-type human papillomavirus infections, high grade cervical, vulvar and vaginal intraepithelial neoplasia and so on. In addition, the quadrivalent vaccine has been shown to prevent genital warts in women and men. The vaccine is most effective when given to human papillomavirus naive girls. The human papillomavirus vaccines have been incorporated into national immunization programs in 22 European countries. Routine vaccination is recommended for girls aged between 9 and 13 years and catch-up vaccination for females between 13 and 25 years of age. There is no excuse not to incorporate the vaccines into the Hungarian national immunization program. Albeit vaccination is expensive, it is cost-effective in the long run definitely. Anyway, vaccination is a matter of the specialty and the national health program, but not of business. We all are obliged to prevent human suffering. Orv. Hetil., 2013, 154, 603–618.
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21

Douvier, S., and S. Dalac. "Infections à papillomavirus." EMC - Maladies Infectieuses 1, no. 4 (November 2004): 235–61. http://dx.doi.org/10.1016/j.emcmi.2004.08.001.

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22

Krasnopolsky, Vladislav I., Nina V. Zarochentseva, Ksenia V. Krasnopolskaya, Yulia N. Bashankaeva, and Varvara S. Kuzmicheva. "Papillomavirus infection and reproduction." Annals of the Russian academy of medical sciences 75, no. 3 (August 31, 2020): 189–95. http://dx.doi.org/10.15690/vramn1332.

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The purpose of the review a synthesis of research data on the role of human papillomavirus infection in the reproductive health of women and men. Key Points. Human papillomavirus (HPV) is one of the most common sexually transmitted viruses worldwide. According to the World Health Organization, HPV is the main cause of the development of HPV-associated diseases among both women and men. Viruses are subdivided into HPV with low carcinogenic risk, which cause benign warts, and HPV with high carcinogenic risk, which cause cancer. Different types of human papillomaviruses depending on their characteristic tropism, are divided into skin and mucous types. Viral infection in men leads to a decrease in the quality of sperm (for example, asthenozoospermia) due to apoptosis in sperm cells and due to the development of antisperm immunity. A negative viral effect on the fertility of women is manifested in an increase in the frequency of spontaneous miscarriages and a premature rupture of the amniotic membranes during pregnancy. There is evidence that HPV decreases the number of trophoblastic cells and abnormal trophoblastic-endometrial adhesion is also observed. In trophoblastic cells transfected with high-risk HPV, the level of apoptosis increases. HPV vaccination is safe, and the results show not only protection against HPV-associated diseases in women and men, but also a reduction of gestational complications, reduced preterm birth rates and the protection of newborns from infection.
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23

REID, RICHARD, and MITCHELL D. GREENBERG. "Human Papillomavirus-Related Diseases of the Vulva." Clinical Obstetrics and Gynecology 34, no. 3 (September 1991): 630–50. http://dx.doi.org/10.1097/00003081-199109000-00019.

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REID, RICHARD, and MITCHELL D. GREENBERG. "Human Papillomavirus-Related Diseases of the Vulva." Clinical Obstetrics and Gynecology 34, no. 3 (September 1991): 630–50. http://dx.doi.org/10.1097/00003081-199134030-00019.

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25

Woods, Mark, Sharron Chow, Benjamin Heng, Wendy Glenn, Noel Whitaker, Dale Waring, Jenna Iwasenko, et al. "Detecting Human Papillomavirus in Ocular Surface Diseases." Investigative Opthalmology & Visual Science 54, no. 13 (December 11, 2013): 8069. http://dx.doi.org/10.1167/iovs.13-13140.

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26

Romero-Masters, James C., Paul F. Lambert, and Karl Munger. "Molecular Mechanisms of MmuPV1 E6 and E7 and Implications for Human Disease." Viruses 14, no. 10 (September 28, 2022): 2138. http://dx.doi.org/10.3390/v14102138.

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Human papillomaviruses (HPVs) cause a substantial amount of human disease from benign disease such as warts to malignant cancers including cervical carcinoma, head and neck cancer, and non-melanoma skin cancer. Our ability to model HPV-induced malignant disease has been impeded by species specific barriers and pre-clinical animal models have been challenging to develop. The recent discovery of a murine papillomavirus, MmuPV1, that infects laboratory mice and causes the same range of malignancies caused by HPVs provides the papillomavirus field the opportunity to test mechanistic hypotheses in a genetically manipulatable laboratory animal species in the context of natural infections. The E6 and E7 proteins encoded by high-risk HPVs, which are the HPV genotypes associated with human cancers, are multifunctional proteins that contribute to HPV-induced cancers in multiple ways. In this review, we describe the known activities of the MmuPV1-encoded E6 and E7 proteins and how those activities relate to the activities of HPV E6 and E7 oncoproteins encoded by mucosal and cutaneous high-risk HPV genotypes.
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27

Paietta, Elise N., Simona Kraberger, Melanie Regney, Joy M. Custer, Erin Ehmke, Anne D. Yoder, and Arvind Varsani. "Interspecies Papillomavirus Type Infection and a Novel Papillomavirus Type in Red Ruffed Lemurs (Varecia rubra)." Viruses 16, no. 1 (December 25, 2023): 37. http://dx.doi.org/10.3390/v16010037.

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The Papillomaviridae are a family of vertebrate-infecting viruses of oncogenic potential generally thought to be host species- and tissue-specific. Despite their phylogenetic relatedness to humans, there is a scarcity of data on papillomaviruses (PVs) in speciose non-human primate lineages, particularly the lemuriform primates. Varecia variegata (black-and-white ruffed lemurs) and Varecia rubra (red ruffed lemurs), two closely related species comprising the Varecia genus, are critically endangered with large global captive populations. Varecia variegata papillomavirus (VavPV) types −1 and −2, the first PVs in lemurs with a fully identified genome, were previously characterized from captive V. variegata saliva. To build upon this discovery, saliva samples were collected from captive V. rubra with the following aims: (1) to identify PVs shared between V. variegata and V. rubra and (2) to characterize novel PVs in V. rubra to better understand PV diversity in the lemuriform primates. Three complete PV genomes were determined from V. rubra samples. Two of these PV genomes share 98% L1 nucleotide identity with VavPV2, denoting interspecies infection of V. rubra by VavPV2. This work represents the first reported case of interspecies PV infection amongst the strepsirrhine primates. The third PV genome shares <68% L1 nucleotide identity with that of all PVs. Thus, it represents a new PV species and has been named Varecia rubra papillomavirus 1 (VarPV1). VavPV1, VavPV2, and VarPV1 form a new clade within the Papillomaviridae family, likely representing a novel genus. Future work diversifying sample collection (i.e., lemur host species from multiple genera, sample type, geographic location, and wild populations) is likely to uncover a world of diverse lemur PVs.
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28

King, Renee E., Andrea Bilger, Josef Rademacher, Ella T. Ward-Shaw, Rong Hu, Paul F. Lambert, and Susan L. Thibeault. "A Novel In Vivo Model of Laryngeal Papillomavirus-Associated Disease Using Mus musculus Papillomavirus." Viruses 14, no. 5 (May 8, 2022): 1000. http://dx.doi.org/10.3390/v14051000.

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Recurrent respiratory papillomatosis (RRP), caused by laryngeal infection with low-risk human papillomaviruses, has devastating effects on vocal communication and quality of life. Factors in RRP onset, other than viral presence in the airway, are poorly understood. RRP research has been stalled by limited preclinical models. The only known papillomavirus able to infect laboratory mice, Mus musculus papillomavirus (MmuPV1), induces disease in a variety of tissues. We hypothesized that MmuPV1 could infect the larynx as a foundation for a preclinical model of RRP. We further hypothesized that epithelial injury would enhance the ability of MmuPV1 to cause laryngeal disease, because injury is a potential factor in RRP and promotes MmuPV1 infection in other tissues. In this report, we infected larynges of NOD scid gamma mice with MmuPV1 with and without vocal fold abrasion and measured infection and disease pathogenesis over 12 weeks. Laryngeal disease incidence and severity increased earlier in mice that underwent injury in addition to infection. However, laryngeal disease emerged in all infected mice by week 12, with or without injury. Secondary laryngeal infections and disease arose in nude mice after MmuPV1 skin infections, confirming that experimentally induced injury is dispensable for laryngeal MmuPV1 infection and disease in immunocompromised mice. Unlike RRP, lesions were relatively flat dysplasias and they could progress to cancer. Similar to RRP, MmuPV1 transcript was detected in all laryngeal disease and in clinically normal larynges. MmuPV1 capsid protein was largely absent from the larynx, but productive infection arose in a case of squamous metaplasia at the level of the cricoid cartilage. Similar to RRP, disease spread beyond the larynx to the trachea and bronchi. This first report of laryngeal MmuPV1 infection provides a foundation for a preclinical model of RRP.
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29

Wikstrom, A., G. von Krogh, M. A. Hedblad, and S. Syrjanen. "Papillomavirus-associated balanoposthitis." Sexually Transmitted Infections 70, no. 3 (June 1, 1994): 175–81. http://dx.doi.org/10.1136/sti.70.3.175.

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30

Stanley, Margaret A. "Human papillomavirus vaccines." Reviews in Medical Virology 16, no. 3 (2006): 139–49. http://dx.doi.org/10.1002/rmv.498.

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31

Ames, Alisa, and Patti Gravitt. "Human papillomavirus vaccine update." Current Infectious Disease Reports 9, no. 2 (March 2007): 151–58. http://dx.doi.org/10.1007/s11908-007-0011-6.

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32

Araujo, Maíta Poli de, Henrique Truffa Kleine, Tathiana Rebizzi Parmigiano, Natalia Tavares Gomes, Graziela Pascom Caparroz, Ismael Dale Cotrim Guerreiro da Silva, Manoel João Batista Castello Girão, and Marair Gracio Ferreira Sartori. "Prevalence of sexually transmitted diseases in female athletes in São Paulo, Brazil." Einstein (São Paulo) 12, no. 1 (March 2014): 31–35. http://dx.doi.org/10.1590/s1679-45082014ao2949.

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Objective : To determine the prevalence of sexually transmitted diseases in female athletes. Methods : An observational, cross-sectional study was conducted including 50 female athletes with mean age of 20±3 years. Colposcopy, pap smear, and polymerase chain reaction for Chlamydia trachomatis, human papillomavirus and Neisseria gonorrhoeae were performed. Blood samples were collected to test for the human immunodeficiency virus, syphilis, hepatitis B and C. The athletes presenting clinical diseases or conditions identifiable by laboratory tests were treated and followed up in the unit. Results : Forty-six percent of the participants were unaware of sexually transmitted diseases. The prevalence of sexually transmitted diseases among athletes was 48% (24 cases). Human papillomavirus was the most frequent agent (44%). Considering the human papillomavirus genotypes, subtype 16 was the most prevalent (53%), followed by 11-6 (22%) and 18 (13%). Two athletes tested positive for C. trachomatis. There were no cases diagnosed of infection by N. gonorrhoeae, syphilis, hepatitis B, hepatitis C and human immunodeficiency virus. However, only 26 athletes had been vaccinated for hepatitis B. Conclusion : The prevalence of sexually transmitted diseases in female athletes was high. Primary prevention measures (hepatitis B and human papillomavirus vaccination) and secondary (serology, pap smears) must be offered to this specific group of women. The matter should be further approached in sports.
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33

Lopukhov, P. D., N. I. Briko, A. A. Khaldin, N. N. Tsapkova, and O. V. Lupashko. "PAPILLOMAVIRUS INFECTION: PRINCIPLE CHARACTERISTICS, CLINICAL MANIFESTATIONS, VACCINE PROPHYLAXIS." Journal of microbiology epidemiology immunobiology, no. 1 (February 28, 2016): 71–78. http://dx.doi.org/10.36233/0372-9311-2016-1-71-78.

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Papillomaviruses are a large and diverse group of viruses. It includes approximately 200 fully described types that have been detected in humans. Human papilloma viruses (HPV) are etiologic agents during various benign and malignant lesions of mucous membrane and skin epithelium. Very importantly, persistent HPV infection of certain types is a leading cause of carcinoma of uterine cervix, penis, vulva, vagina, anal canal and fauces (including tongue base and tonsils). HPV infection prophylaxis is the best means to control HPV-conditioned diseases, and vaccination, as had been demonstrated, - the most effective method of its prophylaxis. In this paper principle characteristics and clinical manifestations of papillomavirus infection, as well as effectiveness of vaccination against HPV are examined.
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34

Oriel, J. D. "Human papillomavirus infection." Current Opinion in Infectious Diseases 2, no. 1 (February 1989): 2–6. http://dx.doi.org/10.1097/00001432-198902010-00002.

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35

Oriel, J. D. "Human papillomavirus infection." Current Opinion in Infectious Diseases 3, no. 1 (February 1990): 24–29. http://dx.doi.org/10.1097/00001432-199002000-00005.

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36

Munday, John S., Sarah D. Bond, Susan Piripi, Susannah J. Soulsby, and Matthew A. Knox. "Canis Familiaris Papillomavirus Type 26: A Novel Papillomavirus of Dogs and the First Canine Papillomavirus within the Omegapapillomavirus Genus." Viruses 16, no. 4 (April 12, 2024): 595. http://dx.doi.org/10.3390/v16040595.

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Domestic dogs are currently recognized as being infected by 25 different canine papillomavirus (CPV) types classified into three genera. A short sequence from a novel CPV type was amplified, along with CPV1, from a papilloma (wart) from the mouth of a dog. The entire 7499 bp genome was amplified, and CPV26 contained putative coding regions that were predicted to produce four early proteins and two late ones. The ORF L1 showed less than 62% similarity for all previously sequenced CPV types but over 69% similarity to multiple Omegapapillomavirus types from a variety of Caniform species including the giant panda, Weddel seal, and polar bear. Phylogenetic analysis confirmed CPV26 clusters within the Omegapapillomavirus genus. Specific primers were used to investigate the presence of CPV26 DNA within a series of 37 canine proliferative lesions. CPV26 DNA was amplified from one lesion, a cutaneous papilloma that also contained CPV6. This is the first time a PV type within the Omegapapillomavirus genus has been detected in a non-domestic species and this provides evidence that the omegapapillomaviruses infected a common ancestor of, and then co-evolved with, the Caniform species. Whether CPV26 causes disease is uncertain, but the absence of an E7 protein may suggest low pathogenicity.
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37

Spitzer, Mark, and Burton A. Krumholz. "HUMAN PAPILLOMAVIRUS–RELATED DISEASES IN THE FEMALE PATIENT." Urologic Clinics of North America 19, no. 1 (February 1992): 71–82. http://dx.doi.org/10.1016/s0094-0143(21)00847-8.

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38

Stier, Elizabeth A., and Amy S. Baranoski. "Human papillomavirus-related diseases in HIV-infected individuals." Current Opinion in Oncology 20, no. 5 (September 2008): 541–46. http://dx.doi.org/10.1097/cco.0b013e3283094ed8.

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39

Oriel, J. D. "Sexually transmitted diseases in children: human papillomavirus infection." Sexually Transmitted Infections 68, no. 2 (April 1, 1992): 80–83. http://dx.doi.org/10.1136/sti.68.2.80.

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40

Trofatter, Kenneth F. "Interferon Treatment of Anogenstal Human Papillomavirus—Related Diseases." Dermatologic Clinics 9, no. 2 (April 1991): 343–52. http://dx.doi.org/10.1016/s0733-8635(18)30421-2.

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41

Nuovo, Gerard J. "The Role of Human Papillomavirus in Gynecological Diseases." Critical Reviews in Clinical Laboratory Sciences 37, no. 3 (January 2000): 183–215. http://dx.doi.org/10.1080/10408360091174204.

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42

Forman, David, Catherine de Martel, Charles J. Lacey, Isabelle Soerjomataram, Joannie Lortet-Tieulent, Laia Bruni, Jerome Vignat, et al. "Global Burden of Human Papillomavirus and Related Diseases." Vaccine 30 (November 2012): F12—F23. http://dx.doi.org/10.1016/j.vaccine.2012.07.055.

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43

Faras, Anthony J., and Franklin Pass. "Applications of biotechnology to human-papillomavirus-induced diseases." Clinics in Dermatology 3, no. 4 (October 1985): 200–203. http://dx.doi.org/10.1016/0738-081x(85)90067-7.

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44

Weck, Phillip K., Janet L. Brandsma, and John K. Whisnant. "Interferons in the treatment of human papillomavirus diseases." CANCER AND METASTASIS REVIEW 5, no. 2 (1986): 139–65. http://dx.doi.org/10.1007/bf00046428.

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45

Bousarghin, Latifa, Antoine Touzé, Bernard Yvonnet, and Pierre Coursaget. "Positively charged synthetic peptides from structural proteins of papillomaviruses abrogate human papillomavirus infectivity." Journal of Medical Virology 73, no. 3 (May 24, 2004): 474–80. http://dx.doi.org/10.1002/jmv.20114.

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46

Della Fera, Ashley N., Alix Warburton, Tami L. Coursey, Simran Khurana, and Alison A. McBride. "Persistent Human Papillomavirus Infection." Viruses 13, no. 2 (February 20, 2021): 321. http://dx.doi.org/10.3390/v13020321.

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Persistent infection with oncogenic human papillomavirus (HPV) types is responsible for ~5% of human cancers. The HPV infectious cycle can sustain long-term infection in stratified epithelia because viral DNA is maintained as low copy number extrachromosomal plasmids in the dividing basal cells of a lesion, while progeny viral genomes are amplified to large numbers in differentiated superficial cells. The viral E1 and E2 proteins initiate viral DNA replication and maintain and partition viral genomes, in concert with the cellular replication machinery. Additionally, the E5, E6, and E7 proteins are required to evade host immune responses and to produce a cellular environment that supports viral DNA replication. An unfortunate consequence of the manipulation of cellular proliferation and differentiation is that cells become at high risk for carcinogenesis.
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47

Lehtinen, M. "Preventive human papillomavirus vaccination." Sexually Transmitted Infections 78, no. 1 (February 1, 2002): 4–6. http://dx.doi.org/10.1136/sti.78.1.4.

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48

Doorbar, John. "The papillomavirus life cycle." Journal of Clinical Virology 32 (March 2005): 7–15. http://dx.doi.org/10.1016/j.jcv.2004.12.006.

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49

Derbie, Awoke, Daniel Mekonnen, Gizachew Yismaw, Fantahun Biadglegne, Xaveer Van Ostade, and Tamrat Abebe. "Human papillomavirus in Ethiopia." VirusDisease 30, no. 2 (April 20, 2019): 171–79. http://dx.doi.org/10.1007/s13337-019-00527-4.

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50

Galloway, Denise A. "Papillomavirus vaccines in clinical trials." Lancet Infectious Diseases 3, no. 8 (August 2003): 469–75. http://dx.doi.org/10.1016/s1473-3099(03)00720-5.

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