Abstract
This review focuses on the genetics of human papilloma virus and immune dysregulation in cervical neoplasia. HPV, the putative agent in cervical cancer, is the most prevalent sexually transmitted infection worldwide. Cervical cancer is the second most common malignancy in women globally as well. Cervical neoplasia is increased in immuno- suppressed states, such as systemic lupus erythematosus. HPV has evolved mechanisms to evade the host immune system which are discussed. Malignant transformation from involves three steps: infection of the cervix, viral persistence, and progression to cancer. This process involves activation of viral oncogenes and integration of viral DNA into host genome. Cancer prevention and Screening strategies involve a combination of cervical cytology, high risk HPV testing, and colposcopy. Vaccination is effective in preventing primary HPV infection with the high risk HPV types causing the majority of cervical cancers. Experimental therapeutic vaccines offer new ways to treat cervical neoplasia.
Keywords: Cervical cancer, human papillomavirus, systemic lupus erythematosus, lupus, cancer, cervical neoplasia, HPV Cervical Infection, Immunodysregulation, Neoplasia, human papilloma virus, HPV, malignancy, oncogenes, viral DNA, cytology, Vaccination, uterine cervix, immune system, vulva, penis, human immunodeficiency virus, HIV, atypical glandular cells, intraepithelial lesion, cervical intraepithelial neoplasia, dysplasia, intraepithelial neoplastic lesions, Highly active anti-retroviral therapy (HAART), CD4, cervix/uterine carcinoma, sexually transmitted infection, Chlamydia trachomatis, lactobacillus, squamous cell cervical cancer, cervical adenocarcinoma, Long Control Region, Capsid proteins, S phase, episomal DNA, Toll-like receptor, interleukins, tumor necrosis factor, IFN gamma, CD8 cells, immune response, cyclin-dependent kinase 4, promoter p97, HLA genes, cytotoxic T cell, Pap test, PCR, hybridization, RNA, reverse transcriptase, topisomerase II alpha
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