Subject(s)
Cell-Derived Microparticles/metabolism , Human papillomavirus 11/physiology , Human papillomavirus 6/physiology , Macrophages/virology , Papillomavirus Infections/virology , Cell-Derived Microparticles/ultrastructure , Human papillomavirus 11/ultrastructure , Human papillomavirus 6/ultrastructure , Humans , Macrophages/pathology , Macrophages/ultrastructure , Papillomavirus Infections/pathologyABSTRACT
Cervical cancer is caused by human papillomavirus infection. Most human papillomavirus infection is harmless and clears spontaneously but persistent infection with high-risk human papillomavirus (especially type 16) can cause cancer of the cervix, vulva, vagina, anus, penis, and oropharynx. The virus exclusively infects epithelium and produces new viral particles only in fully mature epithelial cells. Human papillomavirus disrupts normal cell-cycle control, promoting uncontrolled cell division and the accumulation of genetic damage. Two effective prophylactic vaccines composed of human papillomavirus type 16 and 18, and human papillomavirus type 16, 18, 6, and 11 virus-like particles have been introduced in many developed countries as a primary prevention strategy. Human papillomavirus testing is clinically valuable for secondary prevention in triaging low-grade cytology and as a test of cure after treatment. More sensitive than cytology, primary screening by human papillomavirus testing could enable screening intervals to be extended. If these prevention strategies can be implemented in developing countries, many thousands of lives could be saved.
Subject(s)
Human papillomavirus 11/pathogenicity , Human papillomavirus 16/pathogenicity , Human papillomavirus 18/pathogenicity , Papillomavirus Infections/virology , Uterine Cervical Neoplasms/virology , Cell Transformation, Neoplastic/pathology , Cell Transformation, Viral , Cross-Sectional Studies , Developing Countries , Female , Human papillomavirus 11/immunology , Human papillomavirus 11/ultrastructure , Human papillomavirus 16/immunology , Human papillomavirus 16/ultrastructure , Human papillomavirus 18/immunology , Human papillomavirus 18/ultrastructure , Human papillomavirus 6/immunology , Human papillomavirus 6/pathogenicity , Human papillomavirus 6/ultrastructure , Humans , Mass Screening , Papillomavirus Infections/epidemiology , Papillomavirus Infections/immunology , Papillomavirus Infections/pathology , Papillomavirus Infections/prevention & control , Papillomavirus Vaccines/administration & dosage , Papillomavirus Vaccines/immunology , Uterine Cervical Neoplasms/epidemiology , Uterine Cervical Neoplasms/immunology , Uterine Cervical Neoplasms/pathology , Uterine Cervical Neoplasms/prevention & control , Vaginal Smears , Virus ReplicationABSTRACT
UNLABELLED: Laryngeal papillomatosis is the most frequent benign neoplasia in children. It is caused by HPV 6 and 11. The lesions are exophytic and highly recurrent, compromising the airway mucosa, mainly the larynx. Study design--clinical prospective. AIMS: To show morphologic alterations of the epithelium (light and electron microscopy) in the HPV-6 lesions. METHODS: Specimens of laryngeal lesions obtained during surgery of four children (1 male, 3 female) were submitted to HPV typing (PCR), light microscopy and electron microscopy. RESULTS: In all specimens, HPV type 6 was found. Epithelial projections were found by electron microscopy with superficial cells in desquamation. Light microscopy showed exophytic projections of the keratinized stratified squamous epithelium overlying a fibrovascular core. Koilocytes (vacuolated cells), suggesting the viral infection by HPV, were identified. No alterations were seen in the basement membrane and corion. Ultraestrutural analysis showed vacuolated cells with clear cytoplasmic inclusions, intercellular injuries and widening intercellular spaces. CONCLUSIONS: morphologic alterations of the epithelium in the HPV-6 lesions are superficial, and additional studies including the others HPV types are needed to show the more aggressive and extensive aspect of the disease.
