Virulence of CSFV deficient in IRF3 degradation
نویسندگان
چکیده
4 Nicolas Ruggli*, Artur Summerfield, Ana R. Fiebach, Laurence Guzylack5 Piriou, Oliver Bauhofer, Catherine G. Lamm, Sandro Waltersperger, Keita 6 Matsuno, Luzia Liu, Markus Gerber, Kyung H. Choi, Martin A. Hofmann, 7 Yoshihiro Sakoda, and Jon-Duri Tratschin 8 9 Institute of Virology and Immunoprophylaxis, Mittelhäusern, Switzerland; Department of 10 Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, 11 Japan; Department of Biochemistry & Molecular Biology, The University of Texas 12 Medical Branch at Galveston, TX 77555-0647, USA 13 14
منابع مشابه
Npro of classical swine fever virus contributes to pathogenicity in pigs by preventing type I interferon induction at local replication sites
Classical swine fever (CSF) caused by CSF virus (CSFV) is a highly contagious disease of pigs. The viral protein Npro of CSFV interferes with alpha- and beta-interferon (IFN-α/β) induction by promoting the degradation of interferon regulatory factor 3 (IRF3). During the establishment of the live attenuated CSF vaccine strain GPE-, Npro acquired a mutation that abolished its capacity to bind and...
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Infection with classical swine fever virus (CSFV) is costly to the livestock industry. Several genomic sequences including velogenic strains and low virulent strains have been identified. However, the reasons for the virulence of the virus have remained unclear. Based on selective pattern and pressure strength, we classified all genes of CSFV into three classes. Among these genes, the E2 gene w...
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Virus infection leads to the activation of transcription factor IRF3 and subsequent production of type I inteferons, which induce the transcription of various antiviral genes called interferon stimulated genes (ISGs) to eliminate viral infection. IRF3 activation requires phosphorylation, dimerization and nuclear translocation. However, the mechanisms for the termination of IRF3 activation in nu...
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Transcription factor IRF3-mediated type I interferon induction is essential for antiviral innate immunity. We identified the deSUMOylating enzyme Sentrin/SUMO-specific protease (SENP) 2 as a negative regulator of virus-triggered IFN-β induction. Overexpression of SENP2 caused IRF3 deSUMOylation, K48-linked ubiquitination, and degradation, whereas depletion of SENP2 had opposite effects. Both t...
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تاریخ انتشار 2008