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Updated: Aug 19, 2026

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
Published on: March 8, 2012
Update on pathophysiologic mechanisms of human papillomavirus
1Department of Gynaecology Oncology, Nelson R. Mandela School of Medicine, University of KwaZulu Natal, Congella, Durban, South Africa. moodleym29@ukzn.ac.za
Purpose Of Review:
The role of the human papillomavirus in the pathogenesis has been the subject of many publications in the recent literature. The physical state of the human papillomavirus and the role of chromosomal aneuploidy has been reported. This review discusses the recent pathological mechanisms described in the genesis of human papillomavirus-related disease.
Recent Findings:
The mere presence of the human papillomavirus is not sufficient for the development of neoplasia. Genetic and other co-factors seem to be necessary for the expression of the invasive phenotype. The expression of human papillomavirus 16 E6-E7 oncogenes results in chromosomal aneuploidy, favouring the integration of high-risk human papillomavirus genomes into cellular chromosomes. The integration of human papillomavirus 16 may not always be required for the progression to the invasive phenotype unlike human papillomavirus 18 DNA. Such integration sites are randomly distributed over the whole genome. The genetic susceptibility of codon 98 of the fragile histadine triad has been elucidated.
Summary:
Various molecular mechanisms of human papillomavirus-associated neoplasia are discussed. The interaction between HIV and human papillomavirus are complex and favour the persistence and progression of cervical disease. Future research should pave the way for therapeutic vaccine development.
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