The oral cavity is a common site for human papillomavirus (HPV) infection, however much is still unknown about the spectrum of oral lesions associated with HPV. The prevalence of HPV was investigated in oral dysplasias and papillary lesions using a combination of ISH, p16 and MIB-1 immunohistochemistry. Results show that a subset of high grade oral epithelial dysplasias demonstrated evidence of high-risk HPV infection. Follow-up information suggests a difference in the behaviour of HPV-positive and HPV-negative high grade dysplasias. Oral papillary lesions are a heterogeneous group with variable clinical behaviour. Results support an association of low-risk HPV with papillary lesions that run a benign clinical course, despite the presence of atypia. Other oral papillary lesions with atypical features represent potentially malignant lesions that may progress to carcinoma. Potentially malignant and malignant papillary lesions are not associated with HPV infection. Infection with low versus high-risk HPV results in distinct clinical manifestations.

The oral cavity is a common site for human papillomavirus (HPV) infection, however much is still unknown about the spectrum of oral lesions associated with HPV. The prevalence of HPV was investigated in oral dysplasias and papillary lesions using a combination of ISH, p16 and MIB-1 immunohistochemistry. Results show that a subset of high grade oral epithelial dysplasias demonstrated evidence of high-risk HPV infection. Follow-up information suggests a difference in the behaviour of HPV-positive and HPV-negative high grade dysplasias. Oral papillary lesions are a heterogeneous group with variable clinical behaviour. Results support an association of low-risk HPV with papillary lesions that run a benign clinical course, despite the presence of atypia. Other oral papillary lesions with atypical features represent potentially malignant lesions that may progress to carcinoma. Potentially malignant and malignant papillary lesions are not associated with HPV infection. Infection with low versus high-risk HPV results in distinct clinical manifestations.

Background Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States, and adolescents have the highest incidence. To decrease the burden of HPV and HPV-associated cancers, two vaccines were developed and require a 3 dose series. This study assesses factors that may predict whether a teen will either initiate or complete the vaccine series. Methods National Immunization Survey -Teen 2011 data was used to assess demographic (age, sex, and race/ethnicity) and socioeconomic (poverty and insurance status) factors as they related to vaccine initiation and completion. Bivariate and multivariate analyses were used to determine strength of association. Results Females were more likely than males to initiate and complete the series. Compared to whites, Hispanic teens were 1.5 times more likely to initiate but less likely to complete. Blacks were least likely to complete. Teens below the poverty line were more likely to initiate compared to teens above poverty but less likely to complete. Teens with at least one form of health insurance were 1.2 times more likely to complete than those with no insurance. Conclusion HPV vaccination rates are increasing and need to continue to do so. Emphasis needs to be placed on completing the series to confer complete resistance. This is especially true for blacks and Hispanics who are at a higher risk of HPV-related morbidities.

BACKGROUND: Cervical cancer is a global disease with a disproportionate burden among low- and middle-income countries. In Tanzania, cervical cancer is the most common female cancer and a prophylactic vaccine offering protection against four human papillomavirus (HPV) strains is a promising prevention method. The targeted age and sex, as well as the sexually transmitted nature and novelty of the vaccine, support the need for formative research on the knowledge, attitudes, and barriers toward vaccination. OBJECTIVES: The first objective of this thesis was to systematically review studies of HPV vaccine acceptability among African countries. The second and third objectives were to describe and determine the socio-demographic factors and HPV-related knowledge and attitudes associated with HPV vaccination and to identify the barriers to vaccination among a population-based sample of rural and urban women in the Kilimanjaro Region of Tanzania. METHODS: The literature was systematically reviewed by searching electronic databases, and a data abstraction form structured by the Health Belief Model was used to collect data and synthesize findings. For objectives 2 and 3, a cross-sectional study was conducted among rural (n=303) and urban (n=272) women aged 18-55. Differences in socio-demographic factors, knowledge, attitudes, and barriers were compared between groups, and multivariable models were used to identify associations among rural and urban women separately. RESULTS: Reviewed literature suggested that HPV vaccine-related knowledge was low, however predicted acceptance of the vaccine was high. Research on this topic was largely composed of cross-sectional studies in urban areas. Among rural women in the Kilimanjaro Region, independent associations with acceptance included variables related to cost, knowledge, access, and educational attainment. Among urban women, independent associations were related to social networks/norms and educational attainment. The most frequent perceived barriers to vaccination were cost, side effects, and safety. CONCLUSION: Educational programs on the HPV vaccine and cervical cancer are needed in Tanzania and in other areas of Africa. This research suggests that vaccine campaigns in the Kilimanjaro Region should focus on emphasizing financial and physical accessibility, peer acceptance, and safety, in addition to highlighting endorsement of the vaccine by healthcare providers and the government. / Thesis (Master, Community Health & Epidemiology) -- Queen's University, 2013-10-15 21:01:17.426

Human papillomavirus (HPV) is one of the most common sexually transmitted infections in the United States, however vaccination uptake remains low. One of the known barriers of low vaccination rates is lack of a health care provider recommendation. The purpose of this project was to implement a practice change to increase the number of HPV vaccine recommendations provided by primary care providers (PCPs) to patients aged 9-26 years. The setting for this project was the Little Colorado Physician’s Office, a primary care clinic in rural northern Arizona. Four PCPs, including three family physicians and one family nurse practitioner, and members of the QI team participated in the project. The project was designed as a quality improvement project, guided by the Model for Improvement framework. The needs of the individual practice and their population were assessed by a quality improvement (QI) team using a fishbone diagram for root-cause analysis. A practice change was then implemented by the QI team and evaluated for its effectiveness in improving HPV vaccination recommendations. Outcome measures included the number of HPV vaccine recommendations made by a primary care provider to eligible patients and the number of HPV vaccines administered to patients. In a four-week period of practice change implementation, eight patients were considered eligible for the HPV vaccine. Of these patients, 100% were offered the HPV vaccine by their healthcare provider. The practice change was successful in promoting HPV vaccination recommendations by PCPs, and the QI team reported the change was beneficial to their practice.

Aim: To explore potential methods of increasing cervical screening coverage. Methods: Cervical screening defaulters in Dumfries and Galloway were identified in 2012, split into a control (N=64) and 7 intervention groups who were offered multiple screening options including self-collecting a vaginal sample at home. Self-samples were tested for high-risk human papillomavirus (HPV). A total of 3323 were invited to request a kit and 492 were sent a kit directly. Women who declined screening were asked to complete a questionnaire. Colposcopy referrals from defaulters were audited to identify changes over time. Defaulters attending the hospital smear clinic were questioned to ascertain barriers to cervical screening. Results: Among seven intervention groups the proportion responding varied between 32% (25%-38%) and 14% (11%-17%) compared to 6% among controls. One hundred and thirty women were HPV positive on self-sample, 8 of whom had CIN2+ diagnosed. A significantly higher number of defaulters were referred to colposcopy in June-December 2012 (n=51) than in the same period in 2011 (n=17; OR=3.8, 2.1-6.9). Defaulting was more commonly attributed to practical (112/155=72%) than attitudinal barriers (23/115=15%) (RR=4.9, 3.3-8.0). Conclusions: Practical barriers are often the cause of women not attending for cervical screening and offering more options, particularly the option of self- sampling at home, increases screening coverage.

Human Papillomavirus (HPV) is a small, double stranded DNA tumour virus. Infection with HPV normally results in formation of warts. Certain types of HPV, such as type -16 and -18, are shown to have a causal role in the development of uterine cervical cancer, and are so called high risk type HPV. Recently, a role of HPV in breast cancer has been suggested, although a causal role for HPVs in human breast cancer is yet to be demonstrated. The first part of this study investigates the association of HPV with human breast cancer. The results demonstrate that 48% of breast cancers that occurred in Australian women are HPV positive and they are mainly variants of HPV-18. Further analysis shows that HPV positive breast cancer patients are significantly younger than HPV negative patients, suggesting infection with HPV increases the risk of breast cancer development. This is coincidental with increased risk of HPV infection in sexually active young women and provides evidence that HPV has a role in breast cancer development. The second part of this project investigates the mechanisms by which high risk type HPV oncogenic protein E6, transforms primary human foreskin keratinocytes (natural host cells of HPV). HPV E6 is always expressed in HPV positive cervical carcinoma and results in the degradation of the cellular tumour suppressor protein p53. It is generally believed that HPV E6 contributes to HPV transformation by degradation of p53 protein which leads to cellular immortalisation ? an early step in tumorigenic transformation. Subsequent studies, however, indicate that HPV E6 possesses other functions (such as induction of telomerase activity) which may also be involved in cellular immortalisation. The results of my investigations demonstrate: 1) that degradation of p53 protein is required but is insufficient to immortalise primary cells; 2) that HPV E6 induced telomerase activity is coincidental with an increase in cell culture passage number; 3) that multiple functions of high risk type HPV E6 protein are required for cellular immortalisation. This finding suggests HPV infection is associated with early onset of breast cancer and that multiple functions of high risk type HPV E6 protein are involved in cellular immortalisation. Further study in both of these areas should provide alternative diagnostic markers, leading to prevention and treatment strategies for HPV positive breast cancer and other cancers.

No description available.

While most Human papillomavirus (HPV) infections are asymptomatic and self-resolved, high-risk types, such as HPV-16 and HPV-18 are responsible for 99% of cervical cancers worldwide, whereas low-risk types, such as HPV-6 and HPV-11, are responsible for 90% of genital warts. While the different types of HPV and their varying oncogenicities have been studied extensively, it is still not clear what features of a HPV type make it more oncogenic than another. Two aspects which could affect the oncogenicity of HPV were studied: HPV variants and the E6 protein’s interaction with membrane associated guanylate kinase (MAGUK) proteins. Previous studies have shown that some HPV-16 variants may be more oncogenic than others. The first goal of this work was to characterise the HPV-16 variants in a Manitoba cervical cancer sample population to possibly identify mutations which could be associated with an increased risk of developing cervical cancer. Seventy-five samples from different individuals were sequenced in three distinct regions: the long control region and the E6 and E7 open reading frames. The DNA sequences obtained from these genomic regions were then compared between HPV-16 cervical cancer samples and Manitoba HPV-16 non cancer samples to identify any mutations that were exclusive to the cervical cancer samples. No specific mutations in any of the regions could be associated with cervical cancer. It is also proposed that HPV16 E6 protein’s interaction with MAGUK proteins contributes to its oncogenicity since low-risk E6 proteins lack this ability. The second goal of this work was to investigate which regions of high-risk HPV E6 proteins are needed in order to achieve MAGUK protein degradation, more specifically MAGI-1 degradation. Wild-type high-risk HPV16E6, low-risk HPV6E6, as well as mutants, were synthesized and cloned into vectors. In vitro translated proteins were used in MAGI-1 degradation assays. The ability of both wild-type HPV6 and HPV16 E6 proteins to degrade MAGI-1 was confirmed. Based on the performance of the different mutants in these degradation assays, it was determined that the PDZ-binding domain is necessary but not sufficient to induce E6-induced MAGI-1 degradation. In conclusion, it was determined that the entire HPV16 E6 protein is needed for the induction of MAGI-1 degradation.

The quantification of human papillomavirus (HPV) oncogene transcripts, E6 and E7, may be predictive of viral oncogenesis and cancer progression. The main objectives of this study were to determine the HPV genotype prevalence and distribution in Edmonton, Alberta, and characterize a quantifiable association of HPV E6/E7 mRNA expression with the presence of cervical disease. Successful clinical trial design and patient enrolment lead to the first controlled characterization of HPV genotype epidemiology in Alberta. HPV-16 was identified as the most prevalent genotype, followed by several non-vaccine genotypes (HPV-31, -52). Despite rigorous experimentation and a significant correlation between high-risk HPV infection and cervical lesions (p<0.05), absolute quantification of viral oncogenesis was unsuccessful. The ability to quantify oncogene transcriptional activity may, in time, revolutionize cervical cancer screening programmes, akin to the Pap smear several decades ago. However, as experienced in this study and in others, great challenges and even greater questions remain unanswered.