| Popis: |
The host innate immune response to viral infection often involves the activation of type I interferons (IFNs). Not surprisingly, many viruses have evolved various mechanisms to disable the IFN pathway and evade the antiviral response involving innate immunity. Rabbit hemorrhagic disease (RHD) is caused by RHD virus (RHDV), but whether it can antagonize the production of host IFN to establish infection has not been investigated. In this study, we found that during RHDV infection, the expressions of IFN and the interferon-stimulated gene were not activated. We constructed eukaryotic expression plasmids of all RHDV proteins, and found that RHDV 3C protein inhibited poly(I:C)-induced IFN expressions. Using siRNA to interfere with the expressions of TLR3 and MDA5, we found that the MDA5 signal pathway was used by the 3C protein to inhibit poly(I:C)-induced IFNs expression. This effect was mediated by cleaving the interferon promoter stimulated 1 (IPS-1) protein. Finally, our study showed that IFN was effective against RHDV infection. In summary, our findings showed that RHDV 3C protein was a new interferon antagonist. These results increased our understanding of the escape mechanism from innate immunity mediated by the RHDV 3C protein. |
