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Ciencia Animal ; 31(4):134-153, 2021.
Article in Portuguese | CAB Abstracts | ID: covidwho-1863944
Vet Microbiol ; 252: 108918, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-909094


Porcine haemagglutinating encephalomyelitis virus (PHEV) is a member of coronavirus that causes acute infectious disease and high mortality in piglets. The transcription factor IRF3 is a central regulator of type I interferon (IFN) innate immune signalling. Here, we report that PHEV infection of RAW264.7 cells results in strong suppression of IFN-ß production in the early stage. A comparative analysis of the upstream effector of IFN-ß transcription demonstrated that deactivation of IRF3, but not p65 or ATF-2 proteins, is uniquely attributed to failure of early IFN-ß induction. Moreover, the RIG-I/MDA5/MAVS/TBK1-dependent protective response that regulates the IRF3 pathway is not disrupted by PHEV and works well underlying the deactivated IRF3-mediated IFN-ß inhibition. After challenge with poly(I:C), a synthetic analogue of dsRNA used to stimulate IFN-ß secretion in the TLR-controlled pathway, we show that PHEV and poly(I:C) regulate IFN-ß-induction via two different pathways. Collectively, our findings reveal that deactivation of IRF3 is a specific mechanism that contributes to termination of type I IFN signalling during early infection with PHEV independent of the conserved RIG-I/MAVS/MDA5/TBK1-mediated innate immune response.

Betacoronavirus 1/immunology , Coronavirus Infections/veterinary , Interferon Regulatory Factor-3/genetics , Interferon-beta/immunology , Animals , Betacoronavirus 1/genetics , Coronavirus Infections/immunology , Coronavirus Infections/virology , Immunity, Innate , Interferon Regulatory Factor-3/immunology , Mice , Poly I-C/pharmacology , RAW 264.7 Cells , Signal Transduction/immunology