Abstract
European sea bass (Dicentrarchus labrax) is severely affected 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 different levels of virulence to this fish species. Thus, sea bass is highly susceptible to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fish 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 fish immune response triggered by these viruses have been analysed. Mutated viruses replicated on E-11 cells, although showing some differences compared to the wild type virus, suggesting that the mutations can affect the viral cell recognition and entry. In vivo, fish 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 inflammatory 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.
Highlights
The virulence of a virus depends on several factors related to the pathogen, host, and host-pathogen interaction
A previous study has reported a RGNNV/ SJNNV reassortant strain, isolated from Senegalese sole (Solea senegalensis), which, despite of displaying a SJNNV-type capsid protein (Cp), caused 33% mortality in experimentally infected sea bass[11]. The virulence of this reassortant strain to European sea bass has been proposed to be associated with the presence of RGNNV-type amino acids at positions 247 and 270 of the SJNNV Cp sequence[11]
The infective viral particles obtained after BSRT7/5 cell line transfection were propagated on E-11 cells, recording typical cytopathic effects (CPE) after the first cell inoculation (P0) for rDl965-inoculated cells, whereas one blind passage (P1) was required for cells inoculated with mutant viruses
Summary
The virulence of a virus depends on several factors related to the pathogen, host, and host-pathogen interaction. Two amino acids located in the Cp protruding domain (P-domain) have been suggested as potential betanodavirus virulence determinants[11] Several host factors, such as age, rearing conditions, feeding, and immunological state, may influence the disease severity. A previous study has reported a RGNNV/ SJNNV reassortant strain, isolated from Senegalese sole (Solea senegalensis), which, despite of displaying a SJNNV-type Cp, caused 33% mortality in experimentally infected sea bass[11] The virulence of this reassortant strain to European sea bass has been proposed to be associated with the presence of RGNNV-type amino acids at positions 247 and 270 of the SJNNV Cp sequence (serine in both positions)[11]. The effect of these mutations on viral replication, virulence to sea bass, and host immune response has been analysed
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