A Role for Autophagy in Human Papillomavirus Infection

Cancer is responsible for the death of about 271,520 women in the United States each year. Human papillomaviruses (HPVs) 16, 31, and 33 are the cause of most cervical malignancies. Autophagy, a defense mechanism responsible for cell survival, plays an active role in the progression of cancer. Autophagy is a series of processes involving lysosomal degradation of the cells’ organelles and the removal of intercellular components due to internal and external stressors. Evidence has shown a link between the mechanism of other viral infections such as influenza, HIV and HCV, and the autophagic pathway. Based on this evidence, it is expected that autophagy plays a role in HPV infection. This project aims to determine the role of autophagy during HPV infection. Additional aims will be to determine when autophagy begins during HPV infection and to investigate the role autophagy has on viral replication. The lipidation of LC3 is an indicator that conveys when autophagy is activated. More specifically, the lipidation of LC3-I results in the formation of LC3-II. LC3-II levels will be monitored to determine the effect autophagy has on HPV infection. Western blot analysis will be completed to determine levels of LC3-II lipidation. Luciferase assays will be analyzed to measure the changes in viral infectivity when autophagy is activated. The potential autophagic relationship with HPV infection is important. This study will give us a better understanding of the role of autophagy in HPV infection and may lead to additional therapeutic strategies.