Decreasing salinity of seawater moderates immune response and increases survival rate of giant groupers post betanodavirus infection

• Na+-K+-2Cl− cotransporter isoform 2 (NKCC2) cDNA of giant grouper was cloned.
• Decreasing salinity from 30 to 15 ppt increased survivals of NNV-infected groupers.
• NNV-infected groupers reared at 30-ppt salinity showed high immune response.
• NNV-infected dead groupers reared at 30-ppt salinity had low NNV load in the brain.
• Excess IL-1β gene expression in NNV-infected grouper brain may be the death factor.

Giant groupers (Epinephelus lanceolatus), an important aquaculture fish in Asia, are attacked by nervous necrosis virus (NNV), belonging to betanodavirus. Environmental salinity can affect fish immunity and physiology. We examined whether decreasing salinity from 30 to 15 ppt during acclimation of groupers could affect survival with NNV infection and the associated factors. Although NNV infection decreased muscle moisture, up-regulated the gene expression of Na+-K+-2Cl− cotransporter isoform 2, and elevated plasma cortisol level in groupers, these factors were not related to the higher mortality of groupers reared at 30-ppt salinity (S30-groupers), compared to 15-ppt reared groupers (S15-groupers). Infected S30-groupers exhibited high leukocyte count and innate immune gene expression level. Moreover, NNV-infected dead S30-groupers showed high IL-1β gene expression level but low NNV load in the brain. The high or excess IL-1β gene expression levels in the brain of NNV-infected S30-groupers may be the factor in high mortality.