File:PMC4926186 viruses-08-00166-g002.png

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Attribution 4.0 International (CC BY 4.0)

Summary

Author:Fros JJ, Pijlman GP,Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research, University of Oxford(Openi/National Library of Medicine) Source:https://openi.nlm.nih.gov/detailedresult?img=PMC4926186_viruses-08-00166-g002&query=Alphavirus%20infection&it=xg&req=4&npos=3 Description:viruses-08-00166-f002: Alphavirus nonstructural protein 2 (nsP2) reduces interferon (IFN)-stimulated gene (ISG) expression by inducing transcriptional shutoff via RNA polymerase II (RNA pol II)-mediated host cell transcription by degradation of RNA polymerase subunit RPB1 and blocking the IFN-induced janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Viral envelope (E) proteins activate the unfolded protein response (UPR) in the endoplasmic reticulum (ER) and together with kinases such as protein kinase R (PKR) phosphorylate eukaryotic translation initiation factor 2α (eIF2α). The subsequent induction of stress granules (SG) is inhibited by viral nonstructural protein 3 (nsP3), which sequesters Ras GTPase-activating protein-binding protein (G3BP) into viral granules that favor viral replication. General translational shutoff is additionally induced by alphavirus infection independent of eIF2α phosphorylation. Abbreviations: interferon-α/β receptor (IFNAR); tyrosine kinase (TYK); interferon regulatory factor (IRF); interferon stimulated response element (ISRE).