Interferon (IFN) is a vital antiviral factor in host in the early stages after the viral invasion. Meanwhile, viruses have to survive by taking advantage of the cellular machinery and complete their replication. As a result, viruses evolved several immune escape mechanisms to inhibit host IFN expression. However, the mechanisms used to escape the host's IFN system are still unclear for infectious hematopoietic necrosis virus (IHNV). In this study, we report that the N protein of IHNV inhibits IFN1 production in rainbow trout by degrading the MITA. Firstly, the upregulation of IFN1 promoter activity stimulated by poly I:C was suppressed by IHNV infection. Consistent with this result, the overexpression of the N protein of IHNV blocked the IFN1 transcription that was activated by poly I:C and MITA. Secondly, MITA was remarkably decreased by the overexpression of N protein at the protein level. Further analysis demonstrated that the N protein targeted MITA and promoted the ubiquitination of MITA. Taken together, these data suggested that the production of rainbow trout IFN1 could be suppressed by the N protein of IHNV via degrading MITA.