Antiviral activities of sea perch type I and type II IFNs against RGNNV and their different roles in antigen presentation

Abstract

Viral nervous necrosis disease, caused by nervous necrosis virus (NNV), is one of the most serious diseases in many marine and freshwater fish species worldwide. To better understand the antiviral ability and immunoregulatory function of sea perch (Lateolabrax japonicus) interferon (IFN) to NNV infection, three type I IFN genes (IFNc, IFNd and IFNh) and two type II IFN genes (IFNγ and IFNγ rel) were cloned and characterized in this study. Tissue distribution analysis showed that all five IFNs were high expressed in immune organs of sea perch. The transcription levels of IFNc, IFNd and IFNh were significantly up-regulated in both LJB cells in response to Poly I:C treatment or red-spotted grouper nervous necrosis virus (RGNNV) infection and head kidney leukocytes (HKLs) treated with Poly I:C, while the expression of IFNγ and IFNγ rel were only detected in HKLs. Furthermore, promoter activity analysis showed that overexpression of IRF7 significantly enhanced the promoter activities of IFNc, IFNd and IFNh, whereas IRF1 and IRF3 overexpression only induced IFNh promoter activity. In vitro study, IFNc, IFNd, IFNh and IFNγ possessed significant antiviral activities against RGNNV. In addition, overexpressed IFNc and IFNγ up-regulated the expression of antigen presentation cell markers MHCII-α and MHCII-β in LJF cells, indicating IFNc and IFNγ might be involved in antigen presentation. Taken together, our study may provide the basis for exploring the interaction between viruses and the IFN system in sea perch.