Abstract
Human cytomegalovirus (HCMV) is a leading cause of congenital birth defects in the United States. It causes neurological deficits such as deafness, blindness, microcephaly, mental retardation, and cerebral calcification, among others (Cannon 2009). These birth defects are well characterized, but little is known about the mechanisms underlying them. In the present study, we mapped DNA breaks at 1q42, investigated potential sequence changes by incorrect repair, and sought to predict how a viral protein may be interacting with the break sites. To understand how HCMV infection impacts the brain of a developing fetus, we used cerebral organoids. Uninfected organoids were characterized by the morphology and protein expression of their internal structures. We determined that organoids could be infected with HCMV and found abnormal beta tubulin III staining in areas of viral antigen positivity, as well as a decrease in nidogen-1 expression.