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Journal articles on the topic 'Human papillomavirus'

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Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Tong, Yan, Philip Tonui, Aaron Ermel, Omenge Orang’o, Nelson Wong, Maina Titus, Stephen Kiptoo, Kapten Muthoka, Patrick J. Loehrer, and Darron R. Brown. "Persistence of oncogenic and non-oncogenic human papillomavirus is associated with human immunodeficiency virus infection in Kenyan women." SAGE Open Medicine 8 (January 2020): 205031212094513. http://dx.doi.org/10.1177/2050312120945138.

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Objectives: Cervical cancer is caused by persistent infection with oncogenic, or “high-risk” types of human papillomaviruses, and is the most common malignancy in Kenyan women. A longitudinal study was initiated to investigate factors associated with persistent human papillomavirus detection among HIV-infected and HIV-uninfected Kenyan women without evidence of cervical dysplasia. Methods: Demographic/behavioral data and cervical swabs were collected from HIV-uninfected women (n = 82) and HIV-infected women (n = 101) at enrollment and annually for 2 years. Human papillomavirus typing was performed on swabs (Roche Linear Array). Logistic regression models of human papillomavirus persistence were adjusted for demographic and behavioral characteristics. Results: HIV-infected women were older and less likely to be married and to own a home and had more lifetime sexual partners than HIV-uninfected women. All HIV-infected women were receiving anti-retroviral therapy at enrollment and had satisfactory CD4 cell counts and HIV viral loads. One- and two-year persistent human papillomavirus detection was significantly associated with HIV infection for any human papillomavirus, high-risk human papillomavirus, International Agency for the Research on Cancer-classified high-risk human papillomavirus, and non-oncogenic “low-risk” human papillomavirus. Conclusion: Persistent detection of oncogenic and non-oncogenic human papillomavirus was strongly associated with HIV infection in Kenyan women with re-constituted immune systems based on satisfactory CD4 cell counts. In addition to HIV infection, factors associated with an increased risk of human papillomavirus persistence included a higher number of lifetime sex partners. Factors associated with decreased risk of human papillomavirus persistence included older age and being married. Further studies are needed to identify the immunological defects in HIV-infected women that allow human papillomavirus persistence, even in women receiving effective anti-retroviral therapy. Further studies are also needed to determine the significance of low-risk human papillomavirus persistence in HIV-infected women.

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2

Strauss, Melvin, and A. Bennett Jenson. "Human Papillomavirus in Various Lesions of the Head and Neck." Otolaryngology–Head and Neck Surgery 93, no. 3 (June 1985): 342–46. http://dx.doi.org/10.1177/019459988509300310.

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The association of human papillomavirus with benign and malignant epithelial lesions of the head and neck has been studied by a peroxidase-antiperoxidase technique having immunospecificity against genus-specific structural antigens of the papillomaviruses. More than 360 specimen blocks from 144 patients were evaluated. There was evidence of human papillomavirus antigen in three out of eight patients with childhood-onset laryngeal papillomas (37.5%) and in four out of eight patients with adult-onset papillomas (50%). A patient with an unusual flat, wartlike lesion appearing as an oral cavity leukoplakia had detectable papillomavirus antigen in it. None of the 13 cases of inverting papilloma or any of the malignant lesions studied showed evidence for the presence of papillomavirus antigen. There is currently only suggestive evidence for the oncogenic potential of human papillomavirus in the head and neck.

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3

Buck, Christopher B., Diana V. Pastrana, Douglas R. Lowy, and John T. Schiller. "Efficient Intracellular Assembly of Papillomaviral Vectors." Journal of Virology 78, no. 2 (January 15, 2004): 751–57. http://dx.doi.org/10.1128/jvi.78.2.751-757.2004.

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ABSTRACT Although the papillomavirus structural proteins, L1 and L2, can spontaneously coassemble to form virus-like particles, currently available methods for production of L1/L2 particles capable of transducing reporter plasmids into mammalian cells are technically demanding and relatively low-yield. In this report, we describe a simple 293 cell transfection method for efficient intracellular production of papillomaviral-based gene transfer vectors carrying reporter plasmids. Using bovine papillomavirus type 1 (BPV1) and human papillomavirus type 16 as model papillomaviruses, we have developed a system for producing papillomaviral vector stocks with titers of several billion transducing units per milliliter. Production of these vectors requires both L1 and L2, and transduction can be prevented by papillomavirus-neutralizing antibodies. The stocks can be purified by an iodixanol (OptiPrep) gradient centrifugation procedure that is substantially more effective than standard cesium chloride gradient purification. Although earlier data had suggested a potential role for the viral early protein E2, we found that E2 protein expression did not enhance the intracellular production of BPV1 vectors. It was also possible to encapsidate reporter plasmids devoid of BPV1 DNA sequences. BPV1 vector production efficiency was significantly influenced by the size of the target plasmid being packaged. Use of 6-kb target plasmids resulted in BPV1 vector yields that were higher than those with target plasmids closer to the native 7.9-kb size of papillomavirus genomes. The results suggest that the intracellular assembly of papillomavirus structural proteins around heterologous reporter plasmids is surprisingly promiscuous and may be driven primarily by a size discrimination mechanism.

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4

Awua, Adolf K., Alberto Severini, Edwin K. Wiredu, Edwin A. Afari, Vanessa A. Zubach, and Richard M. K. Adanu. "Self-Collected Specimens Revealed a Higher Vaccine- and Non-Vaccine-Type Human Papillomavirus Prevalences in a Cross-Sectional Study in Akuse." Advances in Preventive Medicine 2020 (January 22, 2020): 1–13. http://dx.doi.org/10.1155/2020/8343169.

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Background. Population-specific epidemiologic data on human Papillomavirus infection, which are limited in most of the SubSaharan African countries, are necessary for effective cervical cancer prevention. This study aimed to generate population-specific data on human Papillomavirus infections, and determine which of these, self-collected and provider-collected specimens, gives a higher estimate of the prevalence of human Papillomaviruses, including vaccine and non-vaccine-type human Papillomavirus. Methods. In this cross-sectional study, following a questionnaire-based collection of epidemiological data, self-, and provider-collected specimens, obtained from women 15−65 years of age, were analysed for human Papillomavirus types by a nested-multiplex polymerase chain reaction, and for cervical lesions by Pap testing. HPV data were categorised according to risk type and vaccine types for further analysis. Results. The difference between the overall human Papillomavirus infection prevalences obtained with the self-collected specimens, 43.1% (95% CI of 38.0–51.0%) and that with the provider-collected samples, 23.3% (95% CI of 19.0–31.0%) were significant (p≤0.001). The prevalence of quadrivalent vaccine-type human Papillomaviruses was 12.3% with self-collected specimens, but 6.0% with provider-collected specimens. For the nonavalent vaccine-types, the prevalences were 26.6% and 16.7% respectively. There were multiple infections involving both vaccine-preventable and nonvaccine preventable high-risk human Papillomavirus genotypes. Conclusion. The Akuse subdistrict can, therefore, be said to have a high burden of human Papillomavirus infections, which included nonvaccine types, as detected with both self-collected and provider-collected specimens. These imply that self-collection is to be given a higher consideration as a means for a population-based high-risk human Papillomavirus infections burdens assessment/screening. Additionally, even with a successful implementation of the HPV vaccination, if introduced in Ghana, there is still the need to continue with the screening of women.

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5

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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6

Antonsson, Annika, and Bengt Göran Hansson. "Healthy Skin of Many Animal Species Harbors Papillomaviruses Which Are Closely Related to Their Human Counterparts." Journal of Virology 76, no. 24 (December 15, 2002): 12537–42. http://dx.doi.org/10.1128/jvi.76.24.12537-12542.2002.

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ABSTRACT Papillomaviruses associated with clinical symptoms have been found in many vertebrate species. In this study, we have used an L1 gene consensus PCR test designed to detect a broad spectrum of human skin papillomaviruses to analyze swab samples from healthy skin of 111 animals belonging to 19 vertebrate species. In eight of the species, papillomavirus DNA was found with the following prevalences: chimpanzees, 9 of 11 samples positive; gorillas, 3 of 4; long-tailed macaques, 14 of 16; spider monkeys, 2 of 2; ruffed lemurs, 1 of 2; cows, 6 of 10; European elks, 4 of 4; aurochs, 1 of 1. In total, 53 new putative animal papillomavirus types were found. The results show that skin papillomaviruses can be detected in healthy skin from many different animal species and are sufficiently related genetically to their human counterparts to be identified by a human skin papillomavirus primer set (FAP59 and FAP64).

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7

Peh, Woei Ling, Kate Middleton, Neil Christensen, Philip Nicholls, Kiyofumi Egawa, Karl Sotlar, Janet Brandsma, et al. "Life Cycle Heterogeneity in Animal Models of Human Papillomavirus-Associated Disease." Journal of Virology 76, no. 20 (October 15, 2002): 10401–16. http://dx.doi.org/10.1128/jvi.76.20.10401-10416.2002.

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ABSTRACT Animal papillomaviruses are widely used as models to study papillomavirus infection in humans despite differences in genome organization and tissue tropism. Here, we have investigated the extent to which animal models of papillomavirus infection resemble human disease by comparing the life cycles of 10 different papillomavirus types. Three phases in the life cycles of all viruses were apparent using antibodies that distinguish between early events, the onset of viral genome amplification, and the expression of capsid proteins. The initiation of these phases follows a highly ordered pattern that appears important for the production of virus particles. The viruses examined included canine oral papillomavirus, rabbit oral papillomavirus (ROPV), cottontail rabbit papillomavirus (CRPV), bovine papillomavirus type 1, and human papillomavirus types 1, 2, 11, and 16. Each papillomavirus type showed a distinctive gene expression pattern that could be explained in part by differences in tissue tropism, transmission route, and persistence. As the timing of life cycle events affects the accessibility of viral antigens to the immune system, the ideal model system should resemble human mucosal infection if vaccine design is to be effective. Of the model systems examined here, only ROPV had a tissue tropism and a life cycle organization that resembled those of the human mucosal types. ROPV appears most appropriate for studies of the life cycles of mucosal papillomavirus types and for the development of prophylactic vaccines. The persistence of abortive infections caused by CRPV offers advantages for the development of therapeutic vaccines.

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8

Alp Avci, Gulcin, and Gulendam Bozdayi. "Human Papillomavirus." Kafkas Journal of Medical Sciences 3, no. 3 (2013): 136–44. http://dx.doi.org/10.5505/kjms.2013.52724.

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9

Richart, Ralph M., and Thomas C. Wright. "Human papillomavirus." Current Opinion in Obstetrics and Gynecology 4, no. 5 (October 1992): 662???669. http://dx.doi.org/10.1097/00001703-199210000-00003.

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10

Fox, Paul A., and Mun-Yee Tung. "Human Papillomavirus." American Journal of Clinical Dermatology 6, no. 6 (2005): 365–81. http://dx.doi.org/10.2165/00128071-200506060-00004.

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11

Brody, Herb. "Human papillomavirus." Nature 488, no. 7413 (August 2012): S1. http://dx.doi.org/10.1038/488s1a.

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12

Pownall, Mark. "Human papillomavirus." Practice Nursing 17, no. 2 (February 2006): 73–76. http://dx.doi.org/10.12968/pnur.2006.17.2.20453.

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13

Cadman, Louise. "Human papillomavirus." Practice Nursing 17, no. 8 (August 2006): 393–95. http://dx.doi.org/10.12968/pnur.2006.17.8.21657.

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14

Richart, Ralph M., Shahla Masood, Kari J. Syrjänen, Pierre Vassilakos, Raymond H. Kaufman, Alexander Meisels, Wlodzimierz T. Olszewski, et al. "Human Papillomavirus." Acta Cytologica 42, no. 1 (1998): 50–58. http://dx.doi.org/10.1159/000331534.

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15

JU??REZ-FIGUEROA, LUIS A., COSETTE M. WHEELER, FELIPE J. URIBE-SALAS, CARLOS J. CONDE-GLEZ, LAURA G. ZAMILPA-MEJ??A, SANTA GARC??A-CISNEROS, and MAURICIO HERN??NDEZ-AVILA. "Human Papillomavirus." Sex Transm Dis 28, no. 3 (March 2001): 125–30. http://dx.doi.org/10.1097/00007435-200103000-00001.

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16

Strand, Anders, and Eva Rylander. "HUMAN PAPILLOMAVIRUS." Dermatologic Clinics 16, no. 4 (October 1998): 817–22. http://dx.doi.org/10.1016/s0733-8635(05)70053-x.

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17

Lavelle, Christopher L. B. "Human papillomavirus." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 93, no. 2 (February 2002): 125. http://dx.doi.org/10.1067/moe.2002.119522.

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18

J Bowden, Sarah, and Maria Kyrgiou. "Human papillomavirus." Obstetrics, Gynaecology & Reproductive Medicine 30, no. 4 (April 2020): 109–18. http://dx.doi.org/10.1016/j.ogrm.2020.02.003.

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19

Lilley, Linda Lane, and Susan Schaffer. "Human papillomavirus." Cancer Nursing 13, no. 6 (December 1990): 366???375. http://dx.doi.org/10.1097/00002820-199012000-00007.

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20

Santa Cruz, D. J. "Human papillomavirus." Archives of Dermatology 127, no. 12 (December 1, 1991): 1828–29. http://dx.doi.org/10.1001/archderm.127.12.1828.

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21

Cruz, Daniel J. Santa. "Human Papillomavirus." Archives of Dermatology 127, no. 12 (December 1, 1991): 1828. http://dx.doi.org/10.1001/archderm.1991.04520010074012.

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22

Androphy, Elliot J. "Human Papillomavirus." Archives of Dermatology 125, no. 5 (May 1, 1989): 683. http://dx.doi.org/10.1001/archderm.1989.01670170097018.

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23

Sharipova, I. P., and E. I. Musabaev. "HUMAN PAPILLOMAVIRUS INFECTION AND CERVICAL CANCER (OWERWIEW)." UZBEK MEDICAL JOURNAL 2, no. 4 (April 30, 2021): 23–29. http://dx.doi.org/10.26739/2181-0664-2021-4-4.

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Viral infections are responsible for 15–20% of all human cancers. Infection with oncogenic viruses can contribute to various stages of carcinogenesis. Despite effective screening methods, cervical cancer continues to be a major public health problem. There are large differences in morbidity and mortality from cervical cancer by geographic region. The age-specific prevalence of HPV varies widely in different populations and has shown two peaks of HPV positiveness in young and older women. Around the world, there have been many studies on the epidemiology of HPV infection and oncogenic properties due to different HPV genotypes. However, there are still many countries where population prevalence has not yet been determined. Moreover, screening strategies for cervical cancer differ from country to country. Organized cervical screening programs are potentially more effectivethan opportunistic screening programs.Key words:Human papillomavirus, cervical cancer, screening, dysplasia

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24

Conway, M. J., and C. Meyers. "Replication and Assembly of Human Papillomaviruses." Journal of Dental Research 88, no. 4 (April 2009): 307–17. http://dx.doi.org/10.1177/0022034509333446.

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Human papillomaviruses (HPVs) are small dsDNA tumor viruses, which are the etiologic agents of most cervical cancers and are associated with a growing percentage of oropharyngeal cancers. The HPV capsid is non-enveloped, having a T=7 icosahedral symmetry formed via the interaction among 72 pentamers of the major capsid protein, L1. The minor capsid protein L2 associates with L1 pentamers, although it is not known if each L1 pentamer contains a single L2 protein. The HPV life cycle strictly adheres to the host cell differentiation program, and as such, native HPV virions are only produced in vivo or in organotypic “raft” culture. Research producing synthetic papillomavirus particles—such as virus-like particles (VLPs), papillomavirus-based gene transfer vectors, known as pseudovirions (PsV), and papillomavirus genome-containing quasivirions (QV)—has bypassed the need for stratifying and differentiating host tissue in viral assembly and has allowed for the rapid analysis of HPV infectivity pathways, transmission, immunogenicity, and viral structure.

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25

Varsani, Arvind, Eric van der Walt, Livio Heath, Edward P. Rybicki, Anna Lise Williamson, and Darren P. Martin. "Evidence of ancient papillomavirus recombination." Journal of General Virology 87, no. 9 (September 1, 2006): 2527–31. http://dx.doi.org/10.1099/vir.0.81917-0.

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An open question amongst papillomavirus taxonomists is whether recombination has featured in the evolutionary history of these viruses. Since the onset of the global AIDS epidemic, the question is somewhat less academic, because immune-compromised human immunodeficiency virus patients are often co-infected with extraordinarily diverse mixtures of human papillomavirus (HPV) types. It is expected that these conditions may facilitate the emergence of HPV recombinants, some of which might have novel pathogenic properties. Here, a range of rigorous analyses is applied to full-genome sequences of papillomaviruses to provide convincing statistical and phylogenetic evidence that evolutionarily relevant papillomavirus recombination can occur.

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26

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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27

HIROMURA, Katsuhiko, Masaharu GUNJI, Masahiko FUJINO, and Masafumi ITO. "Human papillomavirus infection in healthy women in Japan." Journal of the Japanese Society of Clinical Cytology 53, no. 5 (2014): 366–70. http://dx.doi.org/10.5795/jjscc.53.366.

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28

Zhumasheva, Karlygash, Gayane Pogossyan, Baurzhan Zhumashev, and Michael Danilenko. "Genetic condition of human papillomavirus high carcinogenic risk." Bulletin of the Karaganda University. “Biology, medicine, geography Series” 97, no. 1 (March 30, 2020): 29–40. http://dx.doi.org/10.31489/2020bmg1/29-40.

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29

Sano, Takaaki. "Human Papillomavirus (HPV) Infection and Immunohistochemistry." Kitakanto Medical Journal 64, no. 4 (2014): 347–48. http://dx.doi.org/10.2974/kmj.64.347.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1363 (August 2011): 22. http://dx.doi.org/10.2165/00128415-201113630-00083.

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31

Lee, Yu-Jeung. "Human Papillomavirus Vaccine." Biomolecules and Therapeutics 15, no. 3 (September 30, 2007): 133–36. http://dx.doi.org/10.4062/biomolther.2007.15.3.133.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1215 (August 2008): 21. http://dx.doi.org/10.2165/00128415-200812150-00064.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1239 (February 2009): 17. http://dx.doi.org/10.2165/00128415-200912390-00052.

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Garland, Suzanne M., and Jennifer S. Smith. "Human Papillomavirus Vaccines." Drugs 70, no. 9 (June 2010): 1079–98. http://dx.doi.org/10.2165/10898580-000000000-00000.

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35

Atkinson, Stacey. "Human papillomavirus vaccination." Learning Disability Practice 18, no. 4 (May 5, 2015): 11. http://dx.doi.org/10.7748/ldp.18.4.11.s15.

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Park, Jong Sup. "Human Papillomavirus Infection." Journal of the Korean Medical Association 45, no. 4 (2002): 430. http://dx.doi.org/10.5124/jkma.2002.45.4.430.

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Kim, Kyung Hyo. "Human Papillomavirus Vaccine." Journal of the Korean Medical Association 51, no. 2 (2008): 144. http://dx.doi.org/10.5124/jkma.2008.51.2.144.

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Kim, Mi-Kyung, Jae Hong No, and Yong-Sang Song. "Human Papillomavirus Vaccine." Journal of the Korean Medical Association 52, no. 12 (2009): 1180. http://dx.doi.org/10.5124/jkma.2009.52.12.1180.

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Siddiqi, Hasan K., and Paul M. Ridker. "Human Papillomavirus Infection." Circulation Research 124, no. 5 (March 2019): 677–78. http://dx.doi.org/10.1161/circresaha.119.314719.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1288 (February 2010): 22–23. http://dx.doi.org/10.2165/00128415-201012880-00065.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1301 (May 2010): 26. http://dx.doi.org/10.2165/00128415-201013010-00091.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1302 (May 2010): 27. http://dx.doi.org/10.2165/00128415-201013020-00083.

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&NA;. "Human papillomavirus vaccine." Reactions Weekly &NA;, no. 1344 (March 2011): 18. http://dx.doi.org/10.2165/00128415-201113440-00061.

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Laudadio, Jennifer. "Human Papillomavirus Detection." Advances In Anatomic Pathology 20, no. 3 (May 2013): 158–67. http://dx.doi.org/10.1097/pap.0b013e31828d1893.

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Bertram, Cathy C., and Victoria P. Niederhauser. "Understanding Human Papillomavirus." American Journal of Health Education 39, no. 1 (January 2008): 15–24. http://dx.doi.org/10.1080/19325037.2008.10599009.

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Verklan, M. Terese. "Human Papillomavirus Vaccinations." Journal of Perinatal & Neonatal Nursing 30, no. 1 (2016): 80–81. http://dx.doi.org/10.1097/jpn.0000000000000154.

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47

Adimora, Adaora A., and E. Byrd Quinlivan. "Human papillomavirus infection." Postgraduate Medicine 98, no. 3 (September 1995): 109–20. http://dx.doi.org/10.1080/00325481.1995.11946045.

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48

Kahn, Jessica A., and David I. Bernstein. "Human papillomavirus vaccines." Pediatric Infectious Disease Journal 22, no. 5 (May 2003): 443–45. http://dx.doi.org/10.1097/01.inf.0000068036.26828.13.

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Eckert, Linda. "Human Papillomavirus Vaccine." Obstetrics & Gynecology 130, no. 4 (October 2017): 691–92. http://dx.doi.org/10.1097/aog.0000000000002271.

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Hoops, Katherine E. M., and Leo B. Twiggs. "Human Papillomavirus Vaccination." Journal of Lower Genital Tract Disease 12, no. 3 (July 2008): 181–84. http://dx.doi.org/10.1097/lgt.0b013e31815f98b5.

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