scholarly journals Immune response to a recombinant capsid protein of striped jack nervous necrosis virus (SJNNV) in turbot Scophthalmus maximus and Atlantic halibut Hippoglossus hippoglossus, and evaluation of a vaccine against SJNNV

2001 ◽  
Vol 45 ◽  
pp. 33-44 ◽  
Author(s):  
S Húsgard ◽  
S Grotmol ◽  
BK Hjeltnes ◽  
OM Rødseth ◽  
E Biering
Keyword(s):  
Immune Response ◽  
Capsid Protein ◽  
Scophthalmus Maximus ◽  
Atlantic Halibut ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus ◽  
Hippoglossus Hippoglossus ◽  
Turbot Scophthalmus Maximus

Changes in Behaviour of Atlantic Halibut (Hippoglossus hippoglossus) and Turbot (Scophthalmus maximus) Yolk-Sac Larvae Induced by Bacterial Infections

1993 ◽  
Vol 50 (12) ◽  
pp. 2552-2557 ◽  
Author(s):  
Anne Berit Skiftesvik ◽  
Øivind Bergh
Keyword(s):  
Bacterial Infections ◽  
Fish Larvae ◽  
Early Stage ◽  
Scophthalmus Maximus ◽  
Yolk Sac ◽  
Atlantic Halibut ◽  
Hippoglossus Hippoglossus ◽  
Pathogenic Vibrio ◽  
Turbot Scophthalmus Maximus ◽  
Reduced Activity

Eggs of Atlantic halibut (Hippoglossus hippoglossus) and turbot (Scophthalmus maximus) were exposed to Flexibacter ovolyticus and pathogenic Vibrio sp. strains prior to, and during hatching. Activity, buoyancy and mortality of the yolk sac larvae were monitored from hatching until time of first feeding. The halibut larvae showed reduced activity and increased mortality in response to the challenge of bacteria, compared to uninfected control groups. In addition, the infected halibut larvae showed increased specific density compared to the uninfected larvae. These responses were not found for turbot. However, turbot larvae infected with Vibrio anguillarum had lower activity than larvae infected with F. ovolyticus. The reduced activity of halibut larvae occurred 1–2 weeks prior to the increased mortality, allowing infections to be detected at an early stage. The results suggest that the behaviour of fish larvae is influenced by bacterial infection.

In vitro neutralization of nervous necrosis virus by a nanobody binding to the protrusion domain of capsid protein

Aquaculture ◽  
2021 ◽  
pp. 737654
Author(s):  
Song Zhu ◽  
Bo Miao ◽  
Yu-Zhou Zhang ◽  
Wei-Wei Zeng ◽  
De-Shou Wang ◽  
...  
Keyword(s):  
Capsid Protein ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus

scholarly journals Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Patricia Moreno ◽  
Sandra Souto ◽  
Rocio Leiva-Rebollo ◽  
Juan J. Borrego ◽  
Isabel Bandín ◽  
...  
Keyword(s):  
Amino Acids ◽  
Immune Response ◽  
Fish Species ◽  
Sea Bass ◽  
Fish Mortality ◽  
Wild Type Virus ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus ◽  
European Sea Bass

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.

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