Interferon regulatory factors interact with viral M2 gene during murine gammaherpesvirus 68 infection
Abstract
Gammaherpesviruses are enveloped viruses with a large genomic size. Gammaherpesviruses infect most individuals worldwide and this subfamily is represented by human viruses Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV). Studies of gammaherpesviruses have been limited due to the species specificity of EBV and KSHV. Murine gammaherpesvirus 68 (MHV68) has been used as a tractable small animal model to better understand virus-host interactions, antiviral immunity, and pathogenesis. MHV68 is a natural pathogen of wild rodents and upon sequencing has been shown to be closely related to EBV and KSHV. MHV68, like all herpesviruses, has a triphasic life span which includes lytic infection, latent infection, and reactivation. Acute lytic infection is cleared by the innate and adaptive immune response, followed by a lifelong latent infection, and eventual periodic reactivation of lytic viral replication under immunosuppression. What remains unclear is the regulation of latent virus gene expression and reactivation. Interferon alpha/beta (IFNαβ) is part of the innate immune system and has antiviral and immune-stimulating properties. IFNαβ has been shown to have a critical role in the regulation of MHV68 infection. The objective of this work is to further understand the interactions between the host innate immune system and lifelong latent infection. This work has elucidated one of the biochemical mechanisms by which the host cell and virus interact to regulate reactivation.
Degree
M.S.
Advisors
Kirshner, Purdue University.
Subject Area
Molecular biology|Virology|Immunology
Off-Campus Purdue Users:
To access this dissertation, please log in to our
proxy server.