Honors Program


Date of this Version


Document Type



Hogg, E. 2024. How Human Cytomegalovirus UL6 Interacts with the Cellular Genes QSOX1 and F2 to Control Proliferation and Disease. Undergraduate Honors Thesis. University of Nebraska-Lincoln.


Copyright Emily Hogg 2024.


Human cytomegalovirus (HCMV) is a common herpesvirus that infects a majority of the population and can be particularly harmful for immunocompromised individuals and transplant patients. An important aspect of HCMV biology is its ability to become latent and later reactivate, establishing a lifelong infection. The RL11 region of HCMV contains genes including UL7 that are important in latency and activation. UL6 is an RL11 gene with an unknown function. Limited previous data shows interaction of UL6 with cellular genes involved in hemostasis and disease, including QSOX1 and F2. QSOX1 is typically important in controlling cell growth in fibroblasts, an important pathway during both lytic and latent HCMV infection. We hypothesize that UL6 interaction with QSOX1 and the resulting proliferation regulate viral load. F2 encodes for a coagulation factor involved in hemostasis and regulating blood clot formation, and changes in vasculature occur in HCMV disease. Interaction of UL6 with F2 may disrupt coagulation systems and result in increased blood clotting. Abnormal proliferation and hypercoagulation are viral complications, and understanding how UL6 changes these cellular pathways is a potential target for new HCMV treatments. The focus of this study is examining UL6, a currently unstudied gene, to determine its involvement in latency and how it interacts with proteins that are important for the viral lifecycle.

Key Words: human cytomegalovirus (HCMV), latency, reactivation, herpesvirus disease, proliferation, QSOX1