Interplay between Human Cytomegalovirus and Intrinsic/Innate Host Responses: A Complex Bidirectional Relationship

Figure 2

Type I IFN restriction factors that target HCMV. Type I interferons (IFN) are effector molecules of the immune response to virus. This antiviral action is mediated by IFN-stimulated genes. ND10 proteins are induced by IFN and function as part of an intrinsic antiviral defense mechanism of the cell by suppressing viral immediate early (IE) gene expression. The IFN-inducible protein IFI16 interacts with and displaces the transcription factor Sp1 from its DNA cognate element, the IR-1 element, in the viral UL54 promoter. This interaction inhibits the UL54 promoter and decreases HCMV DNA synthesis. The IFN-inducible protein viperin exerts its antiviral effects at a late stage of the HCMV life cycle. During infection, viperin is redistributed from the endoplasmic reticulum (ER) to the Golgi apparatus (TGN, trans Golgi network) and then to cytoplasmic vacuoles that contain gB and pp28.