European sea bass (Dicentrarchus labrax) is severely afected by nervous necrosis disease, caused by
nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous
necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detected in sea bass,
although showing diferent levels of virulence to this fsh species. Thus, sea bass is highly susceptible
to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fsh species. The role
of the capsid protein (Cp) amino acids 247 and 270 in the virulence of a RGNNV isolate to sea bass has
been evaluated by the generation of recombinant RGNNV viruses harbouring SJNNV-type amino acids
in the above mentioned positions (Mut247Dl965, Mut270Dl965 and Mut247+270Dl965). Viral in vitro
and in vivo replication, virus virulence and fsh immune response triggered by these viruses have been
analysed. Mutated viruses replicated on E-11 cells, although showing some diferences compared to the
wild type virus, suggesting that the mutations can afect the viral cell recognition and entry. In vivo, fsh
mortality caused by mutated viruses was 75% lower, and viral replication in sea bass brain was altered
compared to non-mutated virus. Regarding sea bass immune response, mutated viruses triggered a
lower induction of IFN I system and infammatory response-related genes. Furthermore, mutations
caused changes in viral serological properties (especially the mutation in amino acid 270), inducing
higher seroconversion and changing antigen recognition.
