HPV in women

2000

HPV in women Direct skin contact with an HPV infected person is the main way through which genital HPV occurs. The contact areas are the anal, vaginal, and oral sex. The diverse categories of HPV are responsible for the formation of genital warts on the skin. Genital warts are hard and usually rough lumps that become visible on the skin of a sick person. Any sexually active person is prone to acquire the virus and the genital warts. The genital warts in women predominantly appear around or inside the vagina, around or inside the anus, on the vulva, on the groin and on the cervix (Monsonego 37). Classification and morphology The human papilloma viruses are heterogeneous in nature. They affect both the mucosal epithelial tissues and the skin. Besides, they are hugely responsible for causing the cervical carcinogenesis. According to the results of the studies in molecular biology, more than one hundred genotypes of the virus exist in humans. The virus falls under two classifications mainly the low risk HPV (LR-HPV and the high risk HPV (HR-HPV). The low risk HPV is predominant in squamous intraepithelial lesions (LSILs) with low grades and the benign lesions. Meanwhile, the high risk HPV includes the HPV-16 and HPV-18. Other high-risk HPV types include HPV-31, 33, 35, 39, 45, 51, 52, 55, 56, 58, 66, 68, and 70 (Evans and Kaslow 602). The high risk HPV has 80 to 90 per cent prevalence rate in cervical cancer and the squamous intraepithelial lesions (HSILs). In the morphological dimension, the genome of the papilloma virus is covalently circular and closed. Its DNA is double stranded and has a measurement of about 8kbp. All the genes of the papilloma virus are coded in the strands that define DNA. Through this, it utilizes the alternative DNA strand to splice the expression of individual gene. The expression of the papilloma virus has a characteristic of large mRNAs array of cells that code for diverse gene types. Additionally, the HPV has a diameter of 55nm (Evans and Kaslow 602). Molecular Biology and Replication Strategy The HPV contamination begins with the infection of the host cell. This promotes the discharge of the virus from the nucleus. As this happens, there are interactions of many cellular transcription factors. These interactions occur with the viral regulatory region (LRC) that does not code. As a result, the two HPV-16 begin to transcript and transforms earlier genes of E6 and E7. Consequently, the proteins that continue to transform interact with the cellular antioncogenic regulator p53. This action results in the disruption of the cell cycle. The cell cycle is under the regulation of the complexes of cyclin dependent kinases (CDKs) and the cyclins (Evans and Kaslow 692). The CDK complexes always inhibit the action of the cyclin. It is a condition for cells to pass the restriction point of G1 in order for the progression of the cell cycle (Evans and Kaslow 692). Retinoblastoma pockets bacteria, RB, p 107, and p 130 are the ones that regulate this process. There is only an indication in the RB leaving the other pocket proteins with the same functions and activities. In essence, they inactivate and bind up the E2F transcription factors. This leads to the inducement of the S phase genes expression that will trigger a mitogenic signal. This signal leads to the activation of the cyclin D1-CDK6 and cyclin D1-CDK4 complexes. The result of this is the