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Proposed model of IFI16 control on HCMV-induced metabolic changes. Upon HCMV infection, IFI16 forms an inhibitory complex with the transcription factor ChREBP, thereby downmodulating the expression of GLUT4 and reducing glucose consumption. Furthermore, IFI16-ChREBP cooperation leads to decreased expression of genes involved in HCMV-induced lipogenesis, which leads to impaired lipid synthesis and reduced infectivity of viral particles.
