HUMAN PAPILLOMAVIRUS ONCOGENESIS: A NARRATIVE REVIEW

Human papillomavirus (HPV) is a member of the Papillomaviridae family which infects squamous cells and mucous layers of humans. Cancer-causing expression of high-risk HPV-infected cells is an unsuccessful, terminal occasion since most disease cells contain incorporated HPV genomes and do create virus descendants. If the reconciliation of high-risk HPV genomes without a doubt addresses an outcome of HPV E6/E7-incited genomic instability, it gives the idea that such a replication procedure may put high-risk HPVs in a difficult situation contrasted with the generally low-risk HPVs that infect the anogenital mucosa. Low-risk HPV E6 and E7 proteins add to the virus life cycle; however they have a significantly lower changing expression and do not incite genomic instability. Low-risk HPV E7 proteins tie to pRB at a diminished proficiency and do not instigate pRB destabilization. HPV E6 proteins don't proficiently communicate with p53 and are uncouth for p53 debasement. High-risk HPVs can as often as possible continue in an infected host cell at a low duplicate number for quite a long time, regularly without causing clinically obvious injuries. A modest number of basal epithelial cells have attributes of immature microorganisms and continually produce differenciated squamous epithelial cells to keep up the trustworthiness of the epithelium for the duration of the existence of the organic entity. The review aimed to sum up the present status of information in regards to the role of the HPV virus in oncogenesis.