The interferon response is involved in nervous necrosis virus acute and persistent infection in zebrafish infection model.

Betanodavirus, a small positive-sense bipartite RNA virus notoriously affecting marine aquaculture worldwide has been extensively studied in vitro. However, impending studies in elucidating virus-host interactions have been limiting due to the lack of appropriate animal disease models. Therefore, in this study, we have attempted to successfully establish NNV infection in zebrafish (Danio rerio) showing typical NNV symptoms and which could potentially serve as an in vivo model for studying virus pathogenesis. Zebrafish being already a powerful research tool in developmental biology and having its genome completely sequenced by the end of 2007 would expedite NNV research. We have observed viral titers peaked at 3 days post-infection and histological study showing lesions in brain tissues similar to natural host infection. Further, we used this infection model to study the acute and persistence infection during NNV infection. Interestingly, RT-PCR and immunoblotting assays revealed that the acute infection in larvae and juveniles is largely due to inactive interferon response as opposed to activated innate immune response during persistent infection in adult stage. This study is the first to demonstrate NNV infection of zebrafish, which could serve as a potential animal model to study virus pathogenesis and neuron degeneration research.