Newborn infants are particularly vulnerable to neurotropic infections of coxsackievirus which can potentially cause serious central nervous system (CNS) diseases such as meningitis and encephalitis. Coxsackievirus is also capable of persisting in the host CNS for extensive periods of time; however, the mechanism by which the virus evades clearance by the host remains unclear. In vivo models of Coxsackievirus infection have previously revealed that the virus isolated from persistent infection is not infectious, suggesting the evolution of the virus over the course of infection. In order to disaggregate the effects of the adaptive immune response and other complicating factors from the actual infection of the central nervous system, we therefore wish to develop and utilize an in vitro model of Coxsackievirus infection using Neural Progenitor and Stem Cells (NPSCs) and a recombinant Coxsackievirus B3 expressing enhanced GFP (eGFP). In developing and utilizing this model we hope to explore the interaction between the host innate immune response and the virus and the impact of these interactions on the evolution of the virus and the development of disorders in the infected host CNS.