Human cytomegalovirus infection impairs axon formation via repressing glycogen synthase kinase-3β activity-mediated adenosine triphosphate synthesis

Under neurogenic inductive conditions, HCMV infection of SHEDs and SH-SY5Ys caused an increase in Glycogen synthase kinase-3β(GSK-3β) phosphorylation level and a decrease in GSK-3β phosphatase activity. HCMV infection was shown to inhibits GSK-3β activity, suppresses the level of mitochondrial oxidative phosphorylation in cells, reduces ATP production, impedes energy supply during neural differentiation, and inhibits neural differentiation.

Our study sheds light on a molecular mechanism by which crosstalk between protein phosphorylation and oxidative phosphorylation links HCMV infection and neural differentiation and raises a potential strategy for the therapy of congenital HCMV infection.