Viral nervous necrosis (VNN) is a disease that affects farmed fish worldwide. Its etiologic agent is the nervous necrosis virus currently classified into 4 species: SJNNV, RGNNV, TPNNV and BFNNV. In Southern Europe, reassortants between RGNNV and SJNNV have been isolated from VNN outbreaks affecting Senegalese sole and gilthead seabream. The aim of the present study is to identify differentially expressed genes (DEGs) involved in gilthead seabream response against different NNV reassortants.
Gilthead seabream juveniles were challenged by intramuscular injection using the wild-type (wt) strain Ss160.03, a highly virulent reassortant isolated from sole, and an attenuated mutant of this strain. Head-kidney and brain samples were collected at 24, 48 and 72 h post-challenge (hpc). Viral multiplication was analysed by qPCR, and the evaluation of the immune response against the infection was carried out using an OpenArray® with 56 gene targets.
At the end of the experiment, viral multiplication in seabream was higher for the wt reassortant. The number of DEGs detected through the experiment was also higher in the wt-infected animals, being the kinetic of expression different between the organs analysed (early deregulation of genes in head-kidney compared to belated expression in brain). The main differences in gene expression found between fish infected with both reassortants occurred at 72 hpc, being all DEGs up-regulated in wt-infected fish, compared to the downregulation observed within the mutant-infected animals. In addition, the expression of toll-like receptor 9 (tlr9), interleukin 1 beta (il1β), and interferon (ifn) was detected exclusively in brain samples at 72 hpc, and the endothelial leukocyte adhesion molecule (elam) in head-kidney samples at the same time point.
The different profiles of gene regulation detected at 72 hpc in gilthead seabream infected with both viruses could be related to the lower multiplication of the mutant strain.
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