Gynecologic oncology and pathologyUpdate on pathophysiologic mechanisms of human papillomavirusMoodley, ManivasanAuthor Information Department of Gynaecology Oncology, Nelson R. Mandela School of Medicine, University of KwaZulu Natal, Congella, Durban, South Africa Correspondence to Manivasan Moodley, Department of Obstetrics and Gynaecology, Gynaecology Oncology, Nelson R. Mandela School of Medicine, University of KwaZulu Natal, Private Bag 7, Congella, Durban 4000, South Africa Tel: +27 31 260 4428; fax: +27 31 260 4427; e-mail: [email protected] Current Opinion in Obstetrics and Gynecology: February 2005 - Volume 17 - Issue 1 - p 61-64 Buy SDC Abstract 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. Abbreviations CIN: cervical intraepithelial neoplasia; FHIT: fragile histidine triad; HPV: human papillomavirus; TSLC 1: tumour suppressor in lung cancer 1. Copyright © 2005 YEAR Wolters Kluwer Health, Inc. All rights reserved.