It is not known why certain HPV types target skin on the hands or feet, while others attack the cells lining the mouth, and still others the genitalia of both males and females. The most dangerous HPV’s, 16 and 18, are commonly transmitted through sexual contact. These HPV’s can produce two kinds of abnormal tissues, condyloma tissue and dysplasia tissue. Condyloma tissues are the wart-like growths. These warts are usually painless, but can cause some irritation, itching, or burning. This tissue appears like a small, cauliflower-type growth on the skin. It can be treated whenever it flares up, and is non malignant. Dysplastic tissue is the presence of abnormal cells on the surface of the skin. Dysplasia is not cancer, but it is a precursor tissue change prior to malignancy. In one example of a cells’ transition from normal to cancerous, dysplasia can be detected on the female cervix through a Pap smear test (and the following lab histopathology process), or visually can be seen by using a magnifying glass called a colposcope.
While not everything is known about how HPV’s function, scientists know much about the biology of the virus, though we do not completely understand its full life cycle. The virus has eight genes that are categorized as being either early or late, according to the time of their expression in the HPV life cycle. The early genes E1 and E2 are involved in viral genome replication and transcription control. Transcription is the process of constructing a messenger RNA molecule that holds a copy of the genetic information from the DNA. The role of the E4 gene is still not known, but it is thought to promote the productive phase of the papilloma virus life cycle. The E5 gene enhances the activity of epidermal growth factor. E6 and E7 interfere with the host cell’s control of transcription and the cell cycle. The late genes L1 and L2 encode viral capsid proteins used in the construction of new viruses.