Analysis of the antibody response in Atlantic salmon against recombinant VP2 of infectious pancreatic necrosis virus (IPNV)

1998 ◽  
Vol 8 (6) ◽  
pp. 447-456 ◽  
Author(s):  
PETTER FROST ◽  
KNUT BöRSHEIM ◽  
CURT ENDRESEN
Keyword(s):  
Atlantic Salmon ◽  
Antibody Response ◽  
Pancreatic Necrosis ◽  
Infectious Pancreatic Necrosis Virus ◽  
Necrosis Virus ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

Infectious Pancreatic Necrosis Virus in Young Salmonids of the Canadian Maritime Provinces

1969 ◽  
Vol 26 (12) ◽  
pp. 3259-3262 ◽  
Author(s):  
R. M. MacKelvie ◽  
H. Artsob
Keyword(s):  
Tissue Culture ◽  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Infectious Pancreatic Necrosis Virus ◽  
Fish Culture ◽  
Necrosis Virus ◽  
Maritime Provinces ◽  
Viral Hemorrhagic Septicemia ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

Infectious pancreatic necrosis virus was isolated from young salmonids, including Atlantic salmon (Salmo solar), in 9 of the 13 fish culture stations of the Canadian Maritime Provinces. The virus was isolated in tissue culture and identified serologically. There was no evidence of Viral Hemorrhagic Septicemia (Egtved disease).

scholarly journals Infectious Pancreatic Necrosis Virus VP5 Is Dispensable for Virulence and Persistence

2005 ◽  
Vol 79 (14) ◽  
pp. 9206-9216 ◽  
Author(s):  
Nina Santi ◽  
Haichen Song ◽  
Vikram N. Vakharia ◽  
Øystein Evensen
Keyword(s):  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Infectious Pancreatic Necrosis Virus ◽  
Nucleotide Position ◽  
Necrosis Virus ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

ABSTRACT Infectious pancreatic necrosis virus (IPNV) is the causative agent of infectious pancreatic necrosis (IPN) disease in salmonid fish. Recent studies have revealed variation in virulence between isolates of the Sp serotype, associated with certain residues of the structural protein VP2. The isolates are also highly heterogenic in the coding region of the nonstructural VP5 protein. To study the involvement of this protein in the pathogenesis of disease, we generated three recombinant VP5 mutant viruses using reverse genetics. The “wild-type” recombinant NVI15 (rNVI15) virus is virulent, having a premature stop codon at nucleotide position 427, putatively encoding a truncated 12-kDa VP5 protein, whereas rNVI15-15K virus encodes a 15-kDa protein. Recombinant rNVI15-ΔVP5 virus contains a mutation in the initiation codon of the VP5 gene that ablates the expression of VP5. Atlantic salmon postsmolts were challenged to study the virulence characteristics of the recovered viruses in vivo. The role of VP5 in persistent infection was investigated by challenging Atlantic salmon fry with the recovered viruses, as well as with the low-virulence field strain Sp103 and a naturally occurring VP5-deficient mutant of Sp103. The results show that VP5 is not required for viral replication in vivo, and its absence does not alter the virulence characteristics of the virus or the establishment of persistent IPNV infection.

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