THE ROLE OF TYPE I INTERFERONS IN THE HOST CD8+ T CELL RESPONSE DURING GAMMAHERPESVIRUS INFECTION

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-/-).

Grantor dc:publisher

Wake Forest University

Year dc:date.issued

2015

Author dc:creator

• Jennings, Ryan

• herpesviridae

Language dc:language.iso

en

Handle dc:identifier.uri

http://hdl.handle.net/10339/57262

OAI identifier oai:identifier

oai:wakespace.lib.wfu.edu:10339/57262