Correlation of Viral Integration and Viral Load Among HPV 16-Infected Women

摘要

Cervical carcinomas develop slowly from intra-epithelial neoplasia lesions (CIN) which may regress or persist. Several earlier studies have shown that HPV DNA is present as an episomal form in CIN lesions while the principle form of the viral DNA in invasive cancer is integrated. HPV is always integrated in cell lines derived from cervical carcinomas or in cells immortalized by transfection of HPV 16 or HPV 18 DNA. Integration of HPV DNA is considered as an important step in tumour progression. Integration of the viral genome into the cellular DNA can have impact on the initial stage of cell transformation on the maintenance of the transformed phenotype and/or on tumour progression. Integrated viral genome may also lead to the expression of proteins with transforming activity. Viral integration may gain the whole genome of viral transforming genes with a new regulatory mechanism involving either the loss of viral regulatory mechanism or in addition of new ones of cellular origin.