Activation of NADPH Oxidase Complex by ISA Virus Nucleoprotein Overexpression: Alteration of SUMO-1 Protein Levels a Consequence of Cellular Oxidative Stress

The pathogenic mechanism of the infectious salmon anemia virus (ISAv) remains unknown. One methodological approach for solving this unknown is to understand the roles of each viral component separately. Therefore, the present study evaluated the viral nucleoprotein (NP) of ISAv to establish effects to reactive oxygen species (ROS) production and SUMOylation profile balance. Salmon head kidney-1 cells transfected with NP evidenced a strong respiratory burst activation and the genic induction of p47phox, SOD, GLURED, and Bad. Additionally, NPtransfected VERO cells showed alteration in the profile of SUMOylated proteins. Notably, pharmacological inhibition of the NADPH oxidase complex through apocynin blocked ROS production and high NP-mediated cellular ROS levels. These results suggest that the ISAv NP alone can trigger, in transfected cells, a strong production of ROS (able to activate pro-apoptotic marker expressions) and modifications to the post-translational profile mediated by SUMO-1.