instruction:
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Early growth response gene-1 (EGR1) is a multifunctional transcription factor that is implicated in viral infection. In this study, we observed that foot-and-mouth disease virus (FMDV) infection significantly triggered EGR1 expression. Overexpression of EGR1 suppressed FMDV replication in porcine cells, and knockdown of EGR1 considerably promoted FMDV replication. A previously reported FMDV mutant virus (with two amino acids mutations in SAP domain) that displays a strong type I interferon (IFN) induction activity was used in this study. We found that SAP mutant FMDV infection induced a higher expression of EGR1 than wildtype FMDV infection, and also triggered higher IFN and IFN-stimulated genes (ISGs) expression than wildtype FMDV infection. This implied a link between EGR1 and type I IFN signaling. Further study showed that overexpression of EGR1 resulted in Sendai virus (SeV)-induced IFN-stimulated response element (ISRE) and NF-B promoter activation. In addition, the SeV-induced ISGs expression was impaired in EGR1 knockdown cells. EGR1 upregulation promoted type I IFN signaling activation and suppressed FMDV and Seneca Valley virus replication. Suppression of the transcriptional activity of EGR1 did not affect its antiviral effect against FMDV. This study reveals a new mechanism evolved by EGR1 to enhance type I IFN signaling and suppress FMDV replication.
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Citation: Early Growth Response Gene-1 Suppresses Foot-and-Mouth Disease Virus Replication by Enhancing Type I Interferon Pathway Signal Transduction

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Coronavirus particles serve three fundamentally important functions in infection. The virion provides the means to deliver the viral genome across the plasma membrane of a host cell. The virion is also a means of escape for newly synthesized genomes. Lastly, the virion is a durable vessel that protects the genome on its journey between cells. This review summarizes the available X-ray crystallography, NMR, and cryoelectron microscopy structural data for coronavirus structural proteins, and looks at the role of each of the major structural proteins in virus entry and assembly. The potential wider conservation of the nucleoprotein fold identified in the Arteriviridae and Coronaviridae families and a speculative model for the evolution of corona-like virus architecture are discussed.
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Supramolecular Architecture of the Coronavirus Particle

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Viruses are dependent on the cellular translation machinery for protein synthesis. Part of the innate immune response to infection is activation of the stress kinase PKR which phosphorylates the alpha subunit of the initiation factor eIF2. This results in inhibition of translation and is intended to block virus replication. A downstream effect of translational shutoff involves the formation of cytoplasmic granules, termed stress granules (SGs), that contain mRNAs, initiation factors, ribosomal subunits, and other mRNA regulatory proteins. SGs hold mRNAs in a translationally inactive state until cells recover from stress. Recent studies have begun to elucidate the impact of SGs on virus replication. Not surprisingly, viruses from diverse families have been found to modulate SG formation in infected cells by associating with important SG effecter proteins. This review describes the current knowledge on SGs and their interaction with and impact on virus replication. The most highly regulated stage of protein synthesis occurs at the initiation step. The translation initation factor eIF2 plays a crucial role in this process. In non-stressed cells, eIF2 complexed with GDP associates with eIF2B, a nucleotide exchange factor, which exchanges GDP for GTP. This exchange allows the eIF2:GTP complex to associate with initiator methionine tRNA to form ternary complex (eIF2:GTP:tRNA Met ). Ternary complex brings the initiating methionine to the 43S ribosome pre-initiation complex. The 43S complex contains the 40S ribosome and a variety of additional initiation factors that play important roles in translation. The 43S complex then forms the 48S ribosomal complex by binding mRNA, which has itself been activated for translation via association with additional initiation factors. The 60S ribosomal subunit is then recruited, at which point GTP is hydrolyzed to GDP and eIF2:GDP is released from the ribosomal complex to again associate with eIF2B and be recharged with GTP to start the process anew [reviewed in [1, 2] ]. Following cellular stress, the alpha subunit of eIF2 is phosphorylated by one of four stress activated kinases; GCN, which is activated during nutrient starvation, PERK, which is activated following ER stress, HRI, which is activated following oxidative stress and heme deficiency, and PKR, which is activated following virus infection [reviewed in [3] ].
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Stress Granules and Virus Replication HHS Public Access