High risk types of Human Papillomavirus are the causative agents of virtually all cases of cervical cancer, 50-90% of other anogenital cancers and approximately 30% of oral and pharyngeal cancers. The high-risk types encode two viral oncogenes, E6 and E7, which work together to initiate cell transformation. The approximately 50 amino acid product of the E6* transcript is expressed during the early stages of HPV infection. In this study, we found that expression of E6* increased the level of reactive oxygen species (ROS) in both HPV+ and HPV- cells. This increased oxidative stress led to higher levels of DNA damage. The observed increase in ROS may be due to a decrease in cellular anti-oxidant activity, as we found that E6* expression also led to decreased expression of SOD and Gpx, These studies indicate that E6* may play an important role in virus-induced mutagenesis by increasing oxidative stress and DNA damage.
School of Medicine
Duerksen-Hughes, Penelope J.
Payne, Kimberly J.
Reeves, Mark E.
Doctor of Philosophy (PhD)
Year Degree Awarded
Date (Title Page)
Library of Congress/MESH Subject Headings
Human Papillomavirus 16, Papillomavirus Infections, Uterine Cervical Neoplasms, Mouth Neoplasms
Subject - Local
Human Papillomavirus 16, Cervical Cancer, Anogenital Cancer, Oral and Pharyngeal Cancers, Virus-Induced Mutagenesis, Oxidative Stress, DNA Damage
Loma Linda University Libraries
This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.
Williams, Vonetta M., "HPV16 E6* Induces Oxidative Stress and DNA Damage" (2014). Loma Linda University Electronic Theses, Dissertations & Projects. Paper 171.
Loma Linda University Electronic Theses and Dissertations
Loma Linda University. Del E. Webb Memorial Library. University Archives