Cytomegalovirus infection lengthens the cell cycle of granule cell precursors during postnatal cerebellar development.

ABSTRACT: Human cytomegalovirus (HCMV) infection in infants infected in utero can lead to a variety of neurodevelopmental disorders. However, mechanisms underlying altered neurodevelopment in infected infants remain poorly understood. We have previously described a murine model of congenital HCMV infection in which murine CMV (MCMV) spreads hematogenously and establishes a focal infection in all regions of the brain of newborn mice, including the cerebellum. Infection resulted in disruption of cerebellar cortical development characterized by reduced cerebellar size and foliation. This disruption was associated with altered cell cycle progression of the granule cell precursors (GCPs), which are the progenitors that give rise to granule cells (GCs), the most abundant neurons in the cerebellum. In the

SUBMITTER: Sung CYW 

PROVIDER: S-EPMC11382886 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature