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Journal of Virology, July 2005, p. 9206-9216, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9206-9216.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Infectious Pancreatic Necrosis Virus VP5 Is Dispensable for Virulence and Persistence

Nina Santi,1,{dagger} Haichen Song,2,{dagger} Vikram N. Vakharia,2,3 and Øystein Evensen4*

Section for Pathology, National Veterinary Institute, 0033 Oslo, Norway,1 Center for Biosystems Research, University of Maryland Biotechnology Institute,2 Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, Maryland 20742,3 Department of Basic Sciences and Aquatic Medicine, Norwegian School of Veterinary Sciences, 0033 Oslo, Norway4

Received 17 November 2004/ Accepted 28 February 2005

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-{Delta}VP5 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.

* Corresponding author. Mailing address: Department of Basic Sciences and Aquatic Medicine, Norwegian School of Veterinary Science, PO Box 8146 Dep., N-0033 Oslo, Norway. Phone: 47-22597106. Fax: 47-22597310. E-mail: oystein.evensen{at}veths.no.

{dagger} Nina Santi and Haichen Song contributed equally to this work.

Journal of Virology, July 2005, p. 9206-9216, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9206-9216.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hwang, H. J., Moon, C. H., Kim, H. G., Kim, J. Y., Lee, J. M., Park, J. W., Chung, D. K. (2007). Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line. J. Virol. 81: 13816-13824 [Abstract] [Full Text]  
  • Song, H., Santi, N., Evensen, O., Vakharia, V. N. (2005). Molecular Determinants of Infectious Pancreatic Necrosis Virus Virulence and Cell Culture Adaptation. J. Virol. 79: 10289-10299 [Abstract] [Full Text]  


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