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.
","abstract_html":"<p>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.</p>","abstract_has_math":false,"creators":["Williams, Vonetta M."],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Basic Sciences","degree_department":null,"school":null,"contributors":["Duerksen-Hughes, Penelope J.","Brantly, Eileen","Payne, Kimberly J.","Reeves, Mark E.","Soto-Wegner, Ubaldo"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-06-01T07:00:00Z","date_published":"2014-06-01T07:00:00Z","updated_at":"2026-07-24T02:52:15Z","subjects":["Biochemistry","Human Papillomavirus 16; Papillomavirus Infections; Uterine Cervical Neoplasms; Mouth Neoplasms","Human Papillomavirus 16","Cervical Cancer","Anogenital Cancer","Oral and Pharyngeal Cancers","Virus-Induced Mutagenesis","Oxidative Stress","DNA Damage"],"languages":["English"],"rights":["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."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/171","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Duerksen-Hughes, Penelope J.","Brantly, Eileen","Payne, Kimberly J.","Reeves, Mark E.","Soto-Wegner, Ubaldo"]},{"key":"dc:creator","label":"Author","values":["Williams, Vonetta M."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_discipline","label":"Discipline","values":["Basic Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy (PhD)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biochemistry","Human Papillomavirus 16; Papillomavirus Infections; Uterine Cervical Neoplasms; Mouth Neoplasms","Human Papillomavirus 16","Cervical Cancer","Anogenital Cancer","Oral and Pharyngeal Cancers","Virus-Induced Mutagenesis","Oxidative Stress","DNA Damage"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:rights","label":"Dc Rights","values":["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."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/171"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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.
"]},{"key":"dc:title","label":"Title","values":["HPV16 E6* Induces Oxidative Stress and DNA Damage"]}]}],"canonical_facts":{"dc:contributor":["Duerksen-Hughes, Penelope J.","Brantly, Eileen","Payne, Kimberly J.","Reeves, Mark E.","Soto-Wegner, Ubaldo"],"dc:creator":["Williams, Vonetta M."],"dc:description.abstract":["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.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/171"],"dc:language":["English"],"dc:rights":["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."],"dc:subject":["Biochemistry","Human Papillomavirus 16; Papillomavirus Infections; Uterine Cervical Neoplasms; Mouth Neoplasms","Human Papillomavirus 16","Cervical Cancer","Anogenital Cancer","Oral and Pharyngeal Cancers","Virus-Induced Mutagenesis","Oxidative Stress","DNA Damage"],"dc:title":["HPV16 E6* Induces Oxidative Stress and DNA Damage"],"thesis:degree_discipline":["Basic Sciences"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T02:52:15Z"}