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Article Dans Une Revue Journal of Virology Année : 2011

Classical swine fever virus npro limits type I interferon induction in plasmacytoid dendritic cells by interacting with interferon regulatory factor 7

Résumé

Viruses are detected by different classes of pattern recognition receptors that lead to the activation of interferon regulatory factors (IRF) and consequently to the induction of alpha/beta interferon (IFN-/). In turn, efficient viral strategies to escape the type I IFN-induced antiviral mechanisms have evolved. Previous studies established that pestivirus Npro antagonizes the early innate immune response by targeting the transcription factor IRF3 for proteasomal degradation. Here, we report that Npro of classical swine fever virus (CSFV) interacts also with IRF7, another mediator of type I IFN induction. We demonstrate that the Znbinding domain of Npro is essential for the interaction of Npro with IRF7. For IRF3 and IRF7, the DNA-binding domain, the central region, and most of the regulatory domain are required for the interaction with Npro. Importantly, the induction of IRF7-dependent type I IFN responses in plasmacytoid dendritic cells (pDC) is reduced after wild-type CSFV infection compared with infection with virus mutants unable to interact with IRF7. This is associated with lower levels of IRF7 in pDC. Consequently, wild-type but not Npro mutant CSFV-infected pDC show reduced responses to other stimuli. Taken together, the results of this study show that CSFV Npro is capable of manipulating the function of IRF7 in pDC and provides the virus with an additional strategy to circumvent the innate defense.

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Dates et versions

hal-01191121 , version 1 (14-11-2015)

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Ana R Fiebach, Laurence Guzylack-Piriou, Sylvie Python, Artur Summerfield, Nicolas Ruggli. Classical swine fever virus npro limits type I interferon induction in plasmacytoid dendritic cells by interacting with interferon regulatory factor 7. Journal of Virology, 2011, 85 (16), pp.8002-8011. ⟨10.1128/JVI.00330-11⟩. ⟨hal-01191121⟩
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