Porcine bocavirus NP1 protein suppresses type I IFN production by interfering with IRF3 DNA-binding activity.

Type I interferon (IFN) and the IFN-induced cellular antiviral responses are the primary defense mechanisms against viral infection; however, viruses always evolve various mechanisms to antagonize this host's IFN responses. Porcine bocavirus (PBoV) is a newly identified porcine parvovirus. In this study, we found that the nonstructural protein NP1 of PBoV inhibits Sendai virus-induced IFN-β production and the subsequent expression of IFN-stimulating genes (ISGs). Ectopic expression of NP1 significantly impairs IRF3-mediated IFN-β production; however, it does not affect the expression, phosphorylation, and nuclear translocation of IRF3, the most important transcription factor for IFN synthesis. Coimmunoprecipitation and Chromatin immunoprecipitation assays suggested that NP1 interacts with the DNA-binding domain of IRF3, which in turn blocks the association of IRF3 with IFN-β promoter. Together, our findings demonstrated that PBoV encodes an antagonist inhibiting type I IFN production, providing a better understanding of the PBoV immune evasion strategy.