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Title: Human Papillomavirus Infection and Genotype Distribution in Relation to Cervical Cytology Abnormalities and HIV-1 Infection at TikurAnbesa Teaching Hospital, AA, Ethiopia
Authors: MULUKEN, DERESE
Advisors: Dr.Solomon G/Sillasie
Dr. YirgueGebrehiwot
Copyright: Dec-2010
Date Added: 6-May-2012
Abstract: Abstract Human Papillomavirus (HPV) is one of the most common causes of sexually transmitted viral diseases in both men and women worldwide. The prevalence of HPV infection in the general population is estimated to be between 9 and 13 percent worldwide and varies between 1.6 and 25.6 percent by country (Dan et al., 2008). Papillomaviruses are ubiquitous and have been detected in a wide variety of animals as well as in humans and are specific for their respective hosts. More than 200 types of HPV have been recognized on the basis of DNA sequence data showing genomic differences (KyungWon et al., 2007). Of the 200 HPVs approximately 40 types are associated with lower genital tract infection. HPV can infect basal epithelial cells of the skin or inner lining of tissues and are categorized as cutaneous types or mucosal types. Cutaneous types of HPV are epidermitrophic and target the skin of the hands and feet. Mucosal types infect the lining of the mouth, throat, respiratory tract, or anogenital epithelium. Based on their association with cervical cancer and precursor lesions, genital HPVs can also be grouped in to High-risk (oncogenic HPVs) and Low-risk HPV types. Low-risk HPV types include types 6, 11, 42, 43, and 44 and High-risk HPV types include types 16, 18, 31, 33, 34, 35, 39, 45, 51, 52, 56, 58, 59, 66,73 and 82 (Folashade et al., 2007). The 200 genotypes are defined by nucleotide sequence variation of more than 10% compared with other known HPV types in the E6, E7 and L1 open reading frames. Those differing by 2- 10% variations are referred to as subtypes whereas intratype variants may vary up to 2% in the coding region and 5% in the non-coding region when compared to that of prototype, variations are commonly caused by deletions or insertions of nucleotides. The degree of polymorphism varies from type to type in all HPV types. These variants are generally classified and named according to their geographic relatedness. Interest in HPV variants is growing rapidly, as increasing evidence suggests that HPV variants may differ biologically and etiologically (Shailja et al., 2008; Jose et al.,2003). Cervical cancer is the second most common cancer among women world wide (Baseman et al., 2005; Eduardo et al., 2001) and the leading cause of cancer related morbidity and mortality in Ethiopian women with or without HIV infection (WHO 2010). Several epidemiological investigations have documented that more than 90% of cervical cancers and precancerous lesions are attributed to infection with oncogenic HPVs (Baseman et al.,2005). The natural history of cervical cancer involves reversible changes in the cervical tissue from a normal state, in which no neoplastic changes are detected in the squamous epithelium, to varying states of cellular abnormalities that ultimately lead to cervical cancer. This sequence forms the premise on which cytologic screening for cervical cancer is based and corresponds to an underlying multistep carcinogenic process in the development of cervical intraepithelial neoplasia (CIN). Low-grade squamous intraepithelial lesions (LSILs) may progress to high grade SILs (HSILs) and invasive cervical cancer or may regress to a normal state. In Ethiopia, although there is no national cancer registry, data collected from retrospective analysis of medical records have clearly indicated that cervical carcinoma is the most frequent cancer among women of reproductive age group (Dawit et al., 2001; France et al.1999). In Tikur Anbessa Teaching hospital the prevalence of abnormal cervical cytological findings among women presenting for Pap screening was 15-20% (Wondwosen E & Bekure T, Unpublished data). HIV-positive men and women are at increased risk of anogenital and oral HPV infection. The risks for HPV-associated high-grade intra-epithelial neoplasia and cancer are also increased. The prevalence of oral, anal, and cervical HPV infection in HIV-positive individuals compared with HIV-negative individuals increases with progressively lower CD4+ levels, as does incident high grade intraepithelial lesions. Studies have shown that HIV-associated attenuation of HPVspecific immune responses allow for persistence of high-grade intraepithelial lesion and sufficient time for accumulation of genetic changes that are important in progression to cancer. Some have also speculated that HIV infection may increase the oncogenicity of high-risk HPV types; HIV also has a negative impact on recurrence of infection and CIN after treatment (Ferenczy et al., 2003; Suzanne et al., 1999).
URI: http://hdl.handle.net/123456789/2628
Appears in:Thesis - Medical Microbiology

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