Poster Sessions

V -29

Sandra Chapman

S. Chapman, A. McBride

Identifying the cis-elements of the high-risk HPV genome involved in segregation and persistent infection

Only a subset of Human Papillomavirus (HPV) types, known as the high-risk HPV’s, are associated with cervical cancer. The virus infects the cells of the basal layer which are highly proliferative. Throughout the course of multiple cell divisions, the viral genome is maintained at constant copy numbers. This suggests that the virus has developed a mechanism to allow proper segregation of its genome during host cell division. Continued expression of the HPV oncogenes E6 and E7 cause malignant progression. Therefore it is valuable to identify the mechanism by which the HPV genome is able to persist in the infected cell through multiple rounds of cell division. Data from studies on BPV-1 suggest that the viral E2 plays a role in tethering the viral genome to the cellular chromosome during mitosis to ensure proper partitioning. The E2 protein is multifunctional and is known to control transcription and replication by binding to its recognition sequences in the URR. This has complicated the analysis of the role these elements play specifically in genome maintenance. However, by co-transfecting replicons with the regions of interest along with wild-type genomes the necessary viral proteins for replication, E1 and E2, would be provided in trans. Through mutational analysis we are analyzing the role these elements play in the maintenance of HPV 18 genomes.