from Mirko Trilling and Hartmut Hengel writing in Cytomegaloviruses: From Molecular Pathogenesis to Intervention:
Interferons (IFNs) comprise a family of three different subtypes (I, II and III) of related cytokines which share their potent immuno-stimulatory and antiviral function. IFN secretion is initiated by synchronous activation of distinct classes of transcription factors (ATF/cJun, IRFs, NF-κB) upon recognition of conserved pathogen-associated molecular patterns (PAMPs) by germ-line-encoded pathogen recognition receptors (PRRs). Binding of the transcription factors to the ifn-b promoter/enhancer assembles the IFN enhanceosome, leading to IFN transcription. Secreted IFNs signal in an autocrine and paracrine manner via Jak-STAT signal transduction pathways stimulating a far-reaching transcriptional program of >300 differentially expressed genes to orchestrate intrinsic, innate and adaptive immunity. The intimate co-adaptation of cytomegaloviruses with their respective host species led to the evolution of multiple viral countermeasures which mitigate the antiviral effect of IFNs. The number of identified HCMV- and MCMV-encoded gene products interfering with IFN induction, IFN receptor signalling or IFN effector functions, is steadily growing. This review aims to provide a snapshot of our current understanding of the balance of power between pro- and antiviral measures positioned between CMV and the host IFN system. Given the immense selective pressure elicited by IFNs, it is tempting to speculate that IFNs have driven CMV to evolve a high number of antagonistic genes ensuring the complex counterbalance with IFNs and promoting CMV replication in an IFN containing environment. Counterintuitively, CMV appears also to exploit IFN induced transcription to enhance its gene expression under appropriate conditions.
Further reading: Cytomegaloviruses: From Molecular Pathogenesis to Intervention