2026-09-20T15:11:20Zhttps://wakespace.lib.wfu.edu/server/oai/request

oai:null:10339/572622026-09-18T13:18:01Zcom_10339_14934col_10339_38132

Jennings, Ryan 2015-08-25T08:35:34Z 2015-08-25T08:35:34Z 2015 https://wakespace.lib.wfu.edu/handle/10339/57262 The human gammaherpesvirus Epstein-Barr virus (EBV) is associated with multiple forms of cancer. Suppressing gammaherpesvirus reactivation and latency is a potential therapeutic target in the prevention or treatment of EBV-associated cancers. CD8+ T cells are crucial to the control of both lytic and latent gammaherpesvirus infection, as demonstrated in the well-established murine model of EBV, murine herpesvirus 68 (MHV68). Type I interferons (type I IFN) also suppress lytic and latent MHV68 infection, and have been demonstrated to directly and indirectly support antiviral CD8+ T cell development and function in various murine viral infection models. Despite well-established roles for CD8+ T cells in controlling gammaherpesvirus infections, the mechanisms that govern the generation and enhancement of the gammaherpesvirus-specific CD8+ T response are unknown. This study was undertaken to evaluate the role of type I IFNs in MHV68-specific CD8+ T cell expansion, differentiation, and functionality utilizing a murine type I IFN receptor knockout strain (IFNAR1-/-). en Wake Forest University herpesviridae MHV68 mice peritoneum rhadinovirus THE ROLE OF TYPE I INTERFERONS IN THE HOST CD8+ T CELL RESPONSE DURING GAMMAHERPESVIRUS INFECTION Dissertation Barton, Erik S Cline, J. Mark Lyles, Doug S Haas, Karen M Grayson, Jason M Microbiology & Immunology open.access