Cytomegalovirus (CMV) is a highly prevalent β-herpesvirus that infects the majority of the population worldwide. CMV infections are usually asymptomatic, however, in immunocompromised individuals and newborns they can lead to severe sequelae and life-threatening conditions. Congenital CMV infection is the most common congenital infection that can affect brain development and cause severe neurological disabilities. CMV can infect a broad range of cells including neurons, which employ pro-survival strategies to avoid destruction from the immune system. Generally, CD4+ and CD8+ T cells play a crucial role in the control of CMV infection in the brain. Since these cells secrete IFNγ, the objective of this thesis is to determine the role of IFNγ in the control of MCMV infection in neurons, using a mouse model of congenital infection. For this purpose, newborn mice lacking IFNγR in neurons were infected with MCMV and organs were harvested at three timepoints of infection. Viral titers in brain were determined by plaque assay and the percentage of infected neurons was quantified by dual immunohistochemical analysis. Analysis of viral titers was also performed for congenitally infected mice lacking IFNγR in astrocytes. The results of these experiments show that IFNγ does not directly control MCMV infection in neurons and astrocytes, both during, and after resolution of productive infection. These findings add to the understanding of immune responses to CMV infection which is pivotal for development of effective therapies and vaccines and raise new questions on which molecules and cells are involved in the control of CMV infection in neurons.