Intracellular interferon signalling pathways as potential regulators of covalently closed circular DNA in the treatment of chronic hepatitis B

Figure 1 Activation of antiviral interferon-stimulated genes by different interferon subtypes. Different subtypes of interferons (IFNs) bind to their cognate receptors to trigger IFN signalling pathways. The activate janus kinase/signal transducers and activators of transcription-dependent signalling results in the formation of transcription complexes that induce the expression several IFN-stimulated response elements-dependent and gamma activated site-dependent antiviral IFN-stimulated genes (ISGs), which target covalently closed circular DNA (cccDNA) stability and function through a variety of mechanisms. The potency of IFN sub-type for cccDNA degradation or silencing is dependent on the types and number of ISGs induced. IFN: Interferon; TYK2: Tyrosine kinase 2; SOCS: Suppressor of cytokine signalling; PKC-δ: Protein kinase C-delta; IRF: Interferon regulatory factor; JAK: Activate janus kinase; STAT: Signal transducers and activators of transcription; ISGF: Interferon-stimulated gene factor; GAF: Gamma-activated factor; ISGs: Interferon-stimulated genes; ISRE: Interferon-stimulated response elements; GAS: Gamma activated site.