Taken together, our results suggest that the establishment of an NNV virus carrier state involves increased immune gene expression in the head kidney, especially for interferon pathway-related genes and cytokines, as seen in the first part of our analysis, and a more “mechanistic” attempt of the host to control virus infection by de-regulation of regulatory (TRIM16L, TRPM2, MAPKBP1) and myosin genes, as observed on the transcriptome analysis. This evidence concerns the gene TRIM16L and viral infectious disease.