Figure 1

Pictorial representation of un-inhibited Avian avulavirus 1 (APMV-1)-induced type I interferon (IFN) response in waterfowl cells. After the fusion of virion and plasma membrane, the viral RNA enters the cytoplasm, where it is recognized by retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA5), or toll like receptor (TLR) 3 and initiates downstream signaling mediated through mitochondrial antiviral-signaling protein (MAVS). Activated MAVS, stimulate the translocation of interferon regulatory factor 3 (IRF3) to the nucleus, leading to the transcription of type I IFNs (IFN-α and β). These upregulations of IFNs may last for is 8–12 h (early phase). Then, these IFNs stimulate JAK–STAT pathway leading to phosphorylation of STAT1 and STAT2 molecules, which (together with factors that are currently unknown in waterfowl) results in the formation of the IFN-stimulated gene factor 3 (ISGF3) transcription factor complex. This multifunctional transcription factor initiates the transcription of hundreds of IFN-stimulated genes (ISGs), which subsequently establish the antiviral state against the invading viruses. Several well-characterized ISGs are revealed in the figure.