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Peer-reviewedCC BY 4.0Transboundary and emerging diseases

Zebrafish Reveals Genotype‐Specific Differences in Betanodavirus Infection and Host Responses

  • Patricia Moreno1
  • Daniel Álvarez-Torres2
  • Manon Mehraz3
  • Candela Ravina1,2
  • Maxence Frétaud3,4
  • Manuel Marí-Beffa2
  • M. Carmen Alonso1
  • Esther García-Rosado1
  • Christelle Langevin3
  • Julia Béjar2
4 affiliations
  1. 1Facultad de Ciencias Departamento de Microbiología Instituto de Biotecnología y Desarrollo Azul, IBYDA Universidad de Málaga Málaga 29071 Spain uma.es
  2. 2Facultad de Ciencias Departamento de Biología Celular Genética y Fisiología Instituto de Biotecnología y Desarrollo Azul, IBYDA Universidad de Málaga Málaga 29071 Spain uma.es
  3. 3Infectiologie Expérimentale des Rongeurs et des Poissons INRAE Université Paris-Saclay Jouy-en-Josas France universite-paris-saclay.fr
  4. 4INRAE UVSQ Virologie et Immunologie Moléculaires Université Paris-Saclay Jouy-en-Josas France universite-paris-saclay.fr
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Abstract

Fish viral encephalopathy and retinopathy (VER) is a significant infectious disease caused by the nervous necrosis virus (NNV), which affects cultured and wild species. Four NNV genotypes with different virulence in susceptible species have been identified: red‐spotted grouper NNV (RGNNV), striped jack NNV (SJNNV), barfin flounder NNV (BFNNV), and tiger puffer NNV (TPNNV), in addition of reassortment between RGNNV and SJNNV. In light of this threat, zebrafish emerged as a promising model to further characterize these pathogens and identify the cellular and molecular mechanisms responsible for susceptibility/resistance phenotypes. Thus, the aim of the present study was to compare the susceptibility of zebrafish to RGNNV, SJNNV, and RGNNV/SJNNV infection and to characterize the pathogenesis of these isolates in terms of virulence and early innate host immune response. Disease symptoms were recorded in all groups of intracranially infected larvae, and quantification of viral genome evidenced that the three isolates replicate in zebrafish larvae. The highest mortality and proportion of larvae showing disease symptoms were registered in the RGNNV group, where the highest viral replication level was also recorded. Thus, RGNNV seems to be the most virulent isolate for zebrafish larvae. Interestingly, transcriptional patterns of IFN I response and apoptosis genes were similar for RGNNV‐ and RGNNV/SJNNV‐inoculated larvae, being interferon regulatory factor 3, irf3 , and receptor transporter protein 3, rtp3 , the most induced genes, whereas a much lower gene upregulation was recorded in SJNNV‐inoculated larvae. RGNNV infection also induced stronger inflammatory responses, including neutrophil recruitment. RGNNV infection of zebrafish larvae by immersion lead to a significant increase of viral genome; however, the infection was quickly controlled. Infection of juvenile zebrafish with RGNNV by intramuscular injection lead to virus migration to the central nervous system; however, no viral RNA replication was recorded. The potential of zebrafish to study NNV‐host interplay prompts further studies into the underlying mechanisms of these observations, which could contribute to design effective strategies to protect farmed fish susceptible to NNV infections.

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Cite

BibTeXRIS
BibTeX
@article{moreno2026zebrafish,
  title = {{Zebrafish Reveals Genotype‐Specific Differences in Betanodavirus Infection and Host Responses}},
  author = {Patricia Moreno and Daniel Álvarez-Torres and Manon Mehraz and Candela Ravina and Maxence Frétaud and Manuel Marí-Beffa and M. Carmen Alonso and Esther García-Rosado and Christelle Langevin and Julia Béjar},
  journal = {Transboundary and emerging diseases},
  year = {2026},
  month = oct,
  doi = {10.1155/tbed/8111758},
  url = {https://hal.inrae.fr/hal-05845429v1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Zebrafish Reveals Genotype‐Specific Differences in Betanodavirus Infection and Host Responses
AU  - Patricia Moreno
AU  - Daniel Álvarez-Torres
AU  - Manon Mehraz
AU  - Candela Ravina
AU  - Maxence Frétaud
AU  - Manuel Marí-Beffa
AU  - M. Carmen Alonso
AU  - Esther García-Rosado
AU  - Christelle Langevin
AU  - Julia Béjar
PY  - 2026
DA  - 2026/10/30
JO  - Transboundary and emerging diseases
DO  - 10.1155/tbed/8111758
UR  - https://hal.inrae.fr/hal-05845429v1
AB  - Fish viral encephalopathy and retinopathy (VER) is a significant infectious disease caused by the nervous necrosis virus (NNV), which affects cultured and wild species. Four NNV genotypes with different virulence in susceptible species have been identified: red‐spotted grouper NNV (RGNNV), striped jack NNV (SJNNV), barfin flounder NNV (BFNNV), and tiger puffer NNV (TPNNV), in addition of reassortment between RGNNV and SJNNV. In light of this threat, zebrafish emerged as a promising model to further characterize these pathogens and identify the cellular and molecular mechanisms responsible for susceptibility/resistance phenotypes. Thus, the aim of the present study was to compare the susceptibility of zebrafish to RGNNV, SJNNV, and RGNNV/SJNNV infection and to characterize the pathogenesis of these isolates in terms of virulence and early innate host immune response. Disease symptoms were recorded in all groups of intracranially infected larvae, and quantification of viral genome evidenced that the three isolates replicate in zebrafish larvae. The highest mortality and proportion of larvae showing disease symptoms were registered in the RGNNV group, where the highest viral replication level was also recorded. Thus, RGNNV seems to be the most virulent isolate for zebrafish larvae. Interestingly, transcriptional patterns of IFN I response and apoptosis genes were similar for RGNNV‐ and RGNNV/SJNNV‐inoculated larvae, being interferon regulatory factor 3, irf3 , and receptor transporter protein 3, rtp3 , the most induced genes, whereas a much lower gene upregulation was recorded in SJNNV‐inoculated larvae. RGNNV infection also induced stronger inflammatory responses, including neutrophil recruitment. RGNNV infection of zebrafish larvae by immersion lead to a significant increase of viral genome; however, the infection was quickly controlled. Infection of juvenile zebrafish with RGNNV by intramuscular injection lead to virus migration to the central nervous system; however, no viral RNA replication was recorded. The potential of zebrafish to study NNV‐host interplay prompts further studies into the underlying mechanisms of these observations, which could contribute to design effective strategies to protect farmed fish susceptible to NNV infections.
SN  - 1865-1674
SN  - 1865-1682
ER  -