Objectives: MCMV infection in newborn mice induces a strong inflammatory response which leads to the activation of microglia and infiltation of innate immune cells. These immune cells can further produce proinflammatory cytokines, such as TNFα which can then exacerbate cerebellar developmental problems. This is underscored by the finding that the treatment of infected animals with glucocorticoids or blocking of TNFα attenuates neuroinflammation and limits deficits in cerebellar development indicating that host inflammatory responses to MCMV infection, rather than the cytopathic effect of virus on infected cells, are important drivers of deficits in cerebellar development. The exact mechanisms and critical components involved are, however, largely unknown. Our preliminary results indicate the role of NK cells in neuroinflammation following congenital MCMV infection. Therefore, the aim of this study is to determine the role of NK cells in activation of microglia and altered cerebellar development. Material and methods: To gain more insight into the impact of MCMV infection on the microglia we performed RNA-seq and phenotype analysis of these cells by flow cytometry. In addition, we performed immunohistochemical analysis to determine whether microglia can be infected with MCMV. To determine the role of NK cells in neuroinflammation we first determined the kinetics of NK cell infiltration in the brain and performed phenotype analysis of these cells by flow cytometry and their tissue localization by immunohistochemistry. We also determined factors responsible for recruitment of NK cells to the brain. To determine the role of NK cells and IFN-γ in altered cerebellar development we depleted NK cells or neutralize IFN-γ in vivo or use mice that lack IFN-γ receptor on brain resident cells and measure EGL thickness and expression of genes in SHH pathway. In addition, we used the plaque assay to determine the role of NK cells and IFN-γ on the control of MCMV infection in the brain. Results: Here, we show that activated newborn NK and ILC1 cells mediate immunopathology instead of controlling the infection and limiting tissue damage. Immunopathology is preceded by activation of microglia and production of CXCL9 and CXCL10, chemokines that recruit NK/ILC1 cells to the brain of MCMV-infected newborns in a CXCR3-dependent manner. IFNγ released by highly activated, brain infiltrating NK/ILC1 cells is a major contributing factor to the altered cerebellar development. Conclusions: This study is the first to demonstrate the immune-pathogenic action of immature newborn NK/ILC1 cells in the brain following congnital MCMV infection. Thus, this study provides an important contribution to understanding the pathogenesis of cHCMV infection, which can be harnessed to design novel therapeutic targets.