Fig. 1

Schematic of avian metapneumovirus genome structure and virion G. Attachment glycoprotein; F. Fusion protein; M. Matrix protein; P. Phosphoprotein; N. Nucleoprotein; L. Large polymerase protein; M2. Matrix protein 2; SH. Small hydrophobic protein"

Fig. 2

Innate immune response mediated against metapneumovirus infection and viral evasion mechanisms Left: Upon MPV infection, viral genomic ssRNA and dsRNA intermediates are exposed to host innate immune sensors (RIG-I/MDA5 in the cytoplasm or Toll-like receptor TLR3/7/8 in the endoplasm). Activation of these immune sensors initiates a downstream signalling cascade that induces IFN-β gene expression.RIG-I/MDA5 signals through the mitochondrial aptamer MAVS, whereas TLR signals through TRIF/MyD88. Both pathways use common TRAF aptamers to activate transcription factors. TRAF3 acts as an aptamer to activate the TANK/TBK1/IKKε complex, which phosphorylates and subsequently dimerises IRF3, whereas TRAF6 is responsible for activation of the IKK complex, which phosphorylates the typical inhibitor of NF-κB (IκB). The activated transcription factors are translocated into the nucleus to drive IFN-β expression. Right: IFN-β is secreted into the extracellular space and binds to its cognate receptor IFNAR, activating downstream JAK-STAT signalling. The receptor-associated tyrosine kinases Jak1 and Tyk2 are juxtaposed for autophosphorylation and activation.STAT is recruited to the tyrosine kinases and phosphorylated. Phosphorylated STAT1/2 forms the ternary complex ISGF3 with IRF9, which translocates to the nucleus and binds to the ISRE in the promoter region upstream of the ISG gene.ISG gene expression ensues and establishes an antiviral state in the cell.OAS, an example of ISG, produces 2′, 5′-oligoadenylate upon detection of dsRNA (2′, 5′-A) and activates RNase L to cleave viral RNA to produce more RLR ligand, a positive feedback mechanism for IFN production. MPV-encoded proteins shown in red can intervene in host innate immune signalling at different points of action, acting as an escape mechanism to maintain viral replication and transmission."